I would like to thank all the staff at Florimond-Desprez. I particularly thank Ellen Goudemand and Dr. Valerie Laurent for their valuable advice and suggestions, Daphné Verdelet for her precious IT assistance at all times, Michael Cochard for his interest and contribution as a durum wheat breeder, and Denis Beghin for his insight in wheat breeding and for his invaluable help in planning and setting up the experimental trials in Cappelle-en-Pévèle. I extend my thanks to all the members of the Laboratoire Céréales for their assistance in phenotyping the plant material.

I would like to deeply and sincerely thank all my PhD colleagues for their friendship and endless encouragements, Marine Ollier, Almuth Müllner, Pauline Rivière, Dr. Mina Samad Zamini and Sebastian Michel. They have been a major source of support.

I would also like to extend my most heartfelt gratitude to my dear family and friends. I deeply thank my partner, Miki, whose love and faith provided on-going support throughout these years. There are no words to thank him enough and I am eternally grateful for his help.

Résumé

Caractérisation des déterminants génétiques de la résistance à la fusariose chez le blé dur La fusariose de l'épi est une maladie fongique qui touche toutes les cultures de céréales à paille à travers le monde entrainant des baisses de rendements et de la qualité des grains. La fusariose pose également un problème pour la sécurité alimentaire lié à la contamination des grains infectés par des mycotoxines. Le développement de variétés résistantes est considéré comme la méthode la plus efficace et la plus durable pour réduire les dommages causés par la maladie et pour limiter la contamination par les mycotoxines. L'amélioration de la résistance à la fusariose chez le blé dur (Triticum durum Desf.) demeure un défi du fait de son extrême sensibilité à la maladie et de la faible variabilité génétique disponible pour ce caractère.

L'objectif principal de cette thèse a été d'évaluer l'effet de Fhb1, le QTL majeur de résistance à la fusariose chez le blé tendre (Triticum aestivumL.), au sein de fonds génétiques de blé dur élite. Pour cela, trois populations de cartographie, comprenant chacune environ 100 F7-RIL (lignées pures recombinantes ou « recombinant inbred lines »), ont été développées à partir de croisements entre la lignée expérimentale de blé dur DBC-480, portant une introgression de Fhb1, et les cultivars de blé dur Karur, Durobonus et SZD1029K. Les lignées ont été évaluées au champ, sur trois saisons, pour leur résistance globale à la fusariose après inoculation en spray de Fusarium culmorum. Des notations morphologiques (date de floraison, hauteur des plantes) ont également été réalisées afin d'évaluer leur influence sur l'infestation. Les lignées ont été génotypées à l'aide de marqueurs SSR et de marqueurs GBS (génotypage par séquençage ou « genotyping-by-sequencing ») développés par DArTseq. L'analyse de liaison a permis d'identifier des QTL de résistance sur les bras des chromosomes 2BL, 3BS, 4AL, 4BS, 5AL et 6AS. DBC-480 contribuait à l'allèle de résistance à tous ces loci. Le QTL sur 3BS a été détecté au sein des trois populations centré sur l'intervalle de Fhb1, confirmant, pour la première fois, son introgression dans le blé dur. L'évaluation de la résistance à la propagation après inoculation ponctuelle, réalisé au sein d'une des trois populations, a également permis de valider l'effet de Fhb1 sur la résistance de type 2 chez le blé dur. La hauteur des plantes influe fortement sur la résistance globale à la fusariose et, en particulier, l'allèle de nanisme Rht-B1b est associé à une plus grande sensibilité à la maladie dans les trois populations. Cependant, l'effet négatif de Rht-B1b sur la résistance est largement compensé dans les lignées possédant Fhb1. Des lignées semi-naines avec un meilleur niveau de résistance ont été sélectionnées et favoriseront le développement de cultivars de blé dur résistants à la fusariose.

Origin of durum wheat

The evolutionary history of cultivated tetraploid wheat started during the development of agriculture about 10.000 years ago in the Fertile Crescent with the domestication of wild emmer (Triticum dicoccoides (Körn. ex Asch. & Graebn.) Schweinf. 2n=4x=28, genome AABB). Wild emmer is an allotetraploid species that arose between 0.25 and 1.3 million years ago from the natural hybridization of the wild diploid wheat Triticum urartu Thumanjan ex Gandilyan (2n=2x=14, genome AA) [START_REF] Dvorák | The evolution of polyploid wheats: identification of the A genome donor species[END_REF]) and an unknown close relative of Aegilops speltoides Tausch (2n=2x=14, genome SS) which provided the B genome [START_REF] Zohary | Hybridization between amphidiploids and the evolution of polyploids in the wheat (Aegilops-Triticum) group[END_REF][START_REF] Kilian | Independent wheat B and G genome origins in outcrossing Aegilops progenitor haplotypes[END_REF]). The mutation that resulted in non-brittle rachis, allowing efficient harvest without spikes shattering at maturity, led to the first domesticated form of emmer (Triticum dicoccum (Schrank) Schübl., 2n=4x=28, genome AABB) [START_REF] Luo | The structure of wild and domesticated emmer wheat populations, gene flow between them, and the site of emmer domestication[END_REF]). Cultivated hulled emmer was an abundant grain crop until the Bronze Age and spread from the Levantine to the Mediterranean basin and Europe [START_REF] Feldman | Origin of Cultivated Wheat[END_REF]). This species is still grown today albeit on a small scale. The acquisition of the free-threshing trait in further domestication events allowed the emergence of cultivated types, such as durum wheat (Triticum durum Desfs, 2n=4x=28, genome AABB), that gradually replaced emmer wheat.

From the Hellenistic period onwards, durum wheat became a major cultivated crop around the Mediterranean [START_REF] Zohary | Domestication of Plants in the Old World: The origin and spread of domesticated plants in Southwest Asia, Europe, and the Mediterranean Basin[END_REF]. Other free-threshing allotetraploid wheat includes Pollard wheat (Triticum turgidum L.), Polish wheat (Triticum polonicum L.), Khorasan wheat (Triticum turanicum Jakubz.) as well as Persian wheat (Triticum carthlicum Nevski). Common wheat (Triticum aestivum L., 2n=6x=42, genome AABBDD) is a free-threshing allohexaploid wheat that emerged about 8000 years ago, and originated from the hybridization between an allotetraploid wheat of AB genome-composition and the diploid goat grass Aegilops tauschii Coss. which contributed the D genome [START_REF] Mcfadden | The origin of Triticum spelta and its free-threshing hexaploid relatives[END_REF][START_REF] Petersen | Phylogenetic relationships of Triticum and Aegilops and evidence for the origin of the A, B, and D genomes of common wheat (Triticum aestivum)[END_REF][START_REF] Dvorak | The origin of spelt and free-threshing hexaploid wheat[END_REF]. In present times, common wheat dominates wheat production worldwide.

The wheat species form an allopolyploid series (x=7) at different ploidy levels and are largely interfertile. The different steps of domestication as well as the breeding history of durum wheat, marked by intense selection pressure in the last century, have contributed to the reduced level of genetic diversity of the current modern elite durum wheat germplasm [START_REF] Thuillet | Estimation of long-term effective population sizes through the history of durum wheat using microsatellite data[END_REF]. The diversity available in landraces as well as in wild and cultivated related species offers a useful reservoir of genetic variation for durum wheat improvement [START_REF] Feuillet | Cereal breeding takes a walk on the wild side[END_REF].

Economic importance of durum wheat

Wheat is one of the three most important staple foods worldwide together with maize and rice, providing an estimated 20% of all calories consumed by humans. Wheat cultivation occupies more arable land than any other crop and its worldwide production reached 730 million tons in 2015 (International Grains Council). Wheat production encompasses different species, of which common wheat represents the quasi-totality accounting for more than 90% of the total wheat grown worldwide. With a total of 39 million tons produced in 2015, durum wheat accounts for about 5% of the global wheat production. On a global scale, durum wheat can be considered a minor crop but represents the main cultivated crop and the primary staple food of the Mediterranean region where it is traditionally grown.

The major area of durum wheat cultivation is located around the Mediterranean basin, which includes South Europe, West Asia and North Africa, known as the SEWANA region. The European Union contributes to about 22% of the global durum wheat production (Italy, France, Greece and Spain being the major producers) and more than half of the world production is concentrated in the SEWANA region. Other main growing areas are the Northern Plains of the United-States and Canada as well as the desert areas between the United-States and Mexico. North America accounts for about 19% of the durum production but represents up to 80% of the durum wheat exports, directed primarily to the Mediterranean region. Cultivation of durum wheat is also found in Australia, Argentina, Central Europe and the Middle East.

Durum wheat is almost exclusively intended for human consumption making it an economically important crop. Grain quality is an important aspect for durum wheat processing and includes high amount of yellow pigment, protein content, gluten quality, vitreousness as well as a low proportion of diseased kernels (Troccoli et al. 2000). On the international market, high grain quality is sought after for production of premium pasta products. Durum wheat is also consumed in the form of couscous, bulgur and flat durum breads [START_REF] Elias | Breeding efforts to develop Fusarium head blight resistant durum wheat in North Dakota[END_REF].

Fusarium head blight

Fusarium head blight (FHB) is a destructive disease of global importance, affecting durum and bread wheat in most regions where these cereals are cultivated (Parry et al., 1995). The disease was first described by W. G Smith in 1884 using the term "wheat scab" and was later renamed "Fusarium blight" by Atanasoff in 1920 [START_REF] Stack | History of Fusarium Head Blight with Emphasis on North America[END_REF]. The causal agents of FHB encompass more than 19 species from the Microdochium and the Fusarium genera. Among the species of the FHB complex, the most predominant ones are Fusarium graminearum [teleomorph:

Gibberella zeae], Fusarium culmorum [teleomorph unknown], Fusarium avenaceum [teleomorph: Monographella nivalis var. neglecta], with their abundance depending on geographical location and climatic conditions, particularly temperature and moisture (Xu et al. 2005;[START_REF] Xu | Relationship between the fungal complex causing Fusarium head blight of wheat and environmental conditions[END_REF]. F. graminearum is generally prevalent under warm and wet conditions, and is considered the most important species in North America, Central Europe and Australia.

In Northwestern Europe, F. culmorum tends to dominate as it favors cooler and more humid conditions (Parry et al. 1995), although, in the last decade, shifts to a prevalence of F. graminearum has been observed in several regions [START_REF] Waalwijk | Major changes in Fusarium spp. in wheat in the Netherlands[END_REF][START_REF] Jennings | Determination of deoxynivalenol-and nivalenol-producing chemotypes of Fusarium graminearum isolated from wheat crops in England and Wales[END_REF]. While these species appear to predominate, often two or more species coexist within the same field or even within the same plant (Xu et al. 2005;[START_REF] Siou | Interactions between head blight pathogens: Consequences for disease development and toxin production in wheat spikes[END_REF]. F. graminearum and F. culmorum show the highest level of pathogenicity of the different causal agents of FHB in wheat [START_REF] Fernandez | Pathogenicity of Fusarium Species on Different Plant Parts of Spring Wheat Under Controlled Conditions[END_REF]. In addition, the isolates of these two species are all able to produce toxic secondary metabolites including deoxynivalenol (DON), nivalenol and zearalenone that accumulate in infected grains (Wegulo 2012). Due to their importance in both prevalence and disease incidence, F. graminearum and F. culmorum are used predominantly by breeders and researchers in artificially inoculated trials, with the majority of epidemiological researches focusing on F. graminearum solely.

Wheat is particularly susceptible to FHB at flowering time and infection may take place throughout the kernel development stage up to the soft dough stage. Outbreaks are favored by warm temperatures coupled with high humidity in the spring season. The risk of epidemics is further increased when natural inoculum is abundant. FHB pathogens are non-host specific and can survive on many different plants, including cereals such as wheat, durum wheat, triticale, rye and maize, and notably may also live asymptomatic on grass hosts (Parry et al. 1995;[START_REF] Inch | The incidence of Fusarium species recovered from inflorescences of wild grasses in southern Manitoba[END_REF]. They overwinter in structures including sporodochia and perithecia on grass stuble, chaff and corn stalk residues left on the soil surface, as well as on infected grains. The conidia and ascospores produced by the fungi are dispersed by the wind and rain splash until they land on wheat heads serving as primary inoculum (Osborne and Stein 2007) . The infection starts when the spores germinate on the wheat heads and the fungal hyphae colonize the floral cavity. The fungus invades the floret via plant structure that are more prone to penetration including anthers, the surface of the glumes, via the lemma and palea, thinwalled cells at the base of the glumes and through natural openings such as stomates or wounds in the chaff [START_REF] Walter | Action and reaction of host and pathogen during Fusarium head blight disease[END_REF]. At the early stage of infection, the fungus establishes a brief biotrophic relationship with the host, while a shift to necrotrophic phase occurs at more advanced stages, causing host cell death [START_REF] Brown | The infection biology of Fusarium graminearum: Defining the pathways of spikelet to spikelet colonisation in wheat ears[END_REF][START_REF] Kazan | On the trail of a cereal killer: Recent advances in Fusarium graminearum pathogenomics and host resistance[END_REF]). The trichothecene mycotoxins, notably DON, synthesized by the fungus at this stage, act as virulence factors contributing to cell damages (Desmond et al. 2008). The production of DON enables the spreading of the fungus through the rachis and the successful colonization of adjacent florets [START_REF] Bai | Deoxynivalenol-nonproducing Fusarium graminearum causes initial infection, but does not cause disease spread in wheat spikes[END_REF]. The propagation in the rachis leads to vascular dysfunction associated with premature ripening of the spike above the point of infection, also termed as wilting [START_REF] Goswami | Heading for disaster: Fusarium graminearum on cereal crops[END_REF]. The typical symptoms of the disease appear a few days after infection with necrotic lesions on the exterior surfaces of florets and glumes of brownish to dark color which evolve in bleaching of the spikelets. Several spikelets of an infected head may be affected. Over the time of infection, premature bleaching may progress throughout the entire head. Infected spikelets may fail to produce kernels, or may contain partially-filled kernels with an atrophied aspect contributing to a reduction on grain numbers and test weight (Parry et al. 1995;[START_REF] Bushnell | Histology and Physiology of Fusarium Head Blight[END_REF]. Colonization of developing kernels is also associated with mycotoxin accumulation.

The affected grains are shriveled and wilted of white to tan color and are usually referred to as Fusarium-diseased kernels (FDK). Besides, kernels contaminated late in development may appear healthy although they may contain toxins [START_REF] Cowger | Post-anthesis moisture increased Fusarium head blight and deoxynivalenol levels in North Carolina winter wheat[END_REF]Siou et al. 2014).

The damages caused by FHB disease are multiple and result in both direct and indirect economic losses. In severe FHB epidemics, yields can be dramatically reduced and harvest containing damaged-kernels may be downgraded or discarded (McMullen et al. 1997). The disease affects also milling, baking and pasta-making properties due to the destruction of starch granules and storage protein in infected grains (Dexter et al. 1996;Nightingale et al. 1999). The main concern associated with FHB contamination is the accumulation of potent mycotoxins in affected samples. In wheat, the most frequently detected Fusarium mycotoxins are DON and its derivatives. DON acts as an inhibitor of protein synthesis and has been proved to be harmful for both human and livestock health when ingested (Pestka 2010). Many countries have established recommendations or regulations for maximum DON content in cereals and cereal products to insure public health safety. For instance, the European Community enacted a strict maximum level of DON in common wheat and durum wheat of 1.25 and 1.75 ppm, respectively (Official Journal of the European Communities 2007).

Regulations also apply to products such as pasta (0.7 ppm), bread and bakery (0.5 ppm) and infant food (0.2 ppm). Similarly, the Food and Drug Administration of the USA has introduced, since 1993, advisory levels for DON of 1 ppm on finished wheat products intended for human consumption (Guidance for Industry and FDA 2010). Crops that exceeded acceptable DON levels may be devaluated or rejected contributing to further economic losses for wheat growers.

Management of Fusarium head blight

There are three main targets in FHB management: the reduction of the amount of primary inoculum, the prevention of inoculum dispersal and the limitation of infection when inoculum is present (Parry et al. 1995). To date no single solution is available for efficient FHB management and control of disease damages. Strategies available include:

Cultural practices: FHB pathogens over-winter on crop residues left on the soil surface after harvest. These infected plant debris represent the main source of primary inoculum for the following crop. FHB epidemics are therefore promoted by agronomic practices that leave high amount of debris on the soil surface and is further aggravated by slow degrading crop residues which provide a substrate for the pathogen for a longer time [START_REF] Sutton | Epidemiology of wheat head blight and maize ear rot caused by Fusarium graminearum[END_REF][START_REF] Pereyra | Colonization and inoculum production of Gibberella zeae in components of wheat residue[END_REF]Blandino et al. 2010). Dill-Macky and[START_REF] Dill-Macky | The Effect of Previous Crop Residues and Tillage on Fusarium Head Blight of Wheat[END_REF] showed that FHB damages were increased by crop rotations that involved consecutive cultivation of host plants especially wheat after maizeand no or minimum tillage approaches, compared to crop sequences including non-host plants (i.e. wheat after soybean) and conventional tillage practice. Avoiding host plant rotations and burial of infested residues have thus been recommended as good practice to reduce FHB outbreaks. The main limitation of the use of deep plowing is its adverse impact on soil erosion and water conservation, rendering this control method environmentally costly. Current popular farming practices, including the adoption of minimum tillage and cereal rotation, support buildup of Fusarium inoculum and may have contributed to the increase in regional FHB epidemics (McMullen et al. 1997).

Chemical control: Chemical control has become available for wheat growers with fungicides of the demethylation inhibitor class [START_REF] Paul | Efficacy of triazole-based fungicides for Fusarium head blight and deoxynivalenol control in wheat: a multivariate meta-analysis[END_REF]McMullen et al. 2012). Their application decreases FHB severity and DON contamination, especially when applied on cultivars showing some level of resistance [START_REF] Wegulo | Effects of Integrating Cultivar Resistance and Fungicide Application on Fusarium Head Blight and Deoxynivalenol in Winter Wheat[END_REF][START_REF] Willyerd | Efficacy and Stability of Integrating Fungicide and Cultivar Resistance to Manage Fusarium Head Blight and Deoxynivalenol in Wheat[END_REF]. Many challenges are associated with the use of fungicide and include difficult proper application timing, variation in fungicide effectiveness and high economic costs (McMullen et al. 2012).

Disease monitoring: The development of FHB forecasting models that predict the risk of a FHB outbreak may help growers determine if fungicide deployment is justified.

Biological control: Microbial antagonists as biological control agents (BCA) have been investigated for FHB management but none are commercially available yet. BCA can reduce infection pressure when applied on crop residues by lowering over-winter survival of the inoculum and spore production potential [START_REF] Inch | Effect of Trichoderma harzianum on perithecial production of Gibberella zeae on wheat straw[END_REF]. BCA applied directly onto the spikes can contain FHB damages by slowing down disease progression [START_REF] Palazzini | Potential biocontrol agents for Fusarium head blight and deoxynivalenol production in wheat[END_REF][START_REF] Xue | Biological control of fusarium head blight of wheat with Clonostachys rosea strain ACM941[END_REF]. Notwithstanding, BCA have been shown to enhance the efficacy of DMI fungicides. They may be a mean to reduce the amount of chemical product needed to effectively control the disease and represent a promising tool in integrated management (Da [START_REF] Luz | Biological control of Fusarium graminearum[END_REF]McMullen et al. 2012).

Host resistance: The control methods mentioned above are only partially effective and, in the case of high disease pressure, they cannot provide sufficient protection to susceptible cultivars [START_REF] Wegulo | Effects of Integrating Cultivar Resistance and Fungicide Application on Fusarium Head Blight and Deoxynivalenol in Winter Wheat[END_REF]). Host resistance is not only regarded as the most effective and sustainable method for FHB control, but the deployment of resistant cultivars is also essential for efficient integrated management strategies [START_REF] Mcmullen | Integrated strategies for Fusarium head blight management in the United States[END_REF][START_REF] Blandino | Integrated strategies for the control of Fusarium head blight and deoxynivalenol contamination in winter wheat[END_REF]. Since over two decades, breeding efforts have been put towards developing cultivars with improved FHB resistance [START_REF] Anderson | Marker-assisted selection for Fusarium head blight resistance in wheat[END_REF].

At present, a combination of strategies including cultural practices, fungicide application and disease monitoring as well as cultivation of resistant varieties is most promising to reduce the risk of FHB epidemics (Gilbert and Haber 2013;[START_REF] Wegulo | Management of Fusarium head blight of wheat and barley[END_REF].

Breeding for Fusarium head blight resistance

FHB resistance in cereals is a quantitative trait governed by numerous genes (Buerstmayr et al. 2009). Resistance can be classified into two major components: resistance to initial infection (type 1) and resistance to spread of the disease within the spike (type 2) (Schroeder and Christensen 1963). Additional components of resistance have later been described and include resistance to toxin accumulation, resistance to kernel infection and tolerance (Mesterhazy 1995). Expression of FHB resistance is modulated by environmental factors, especially temperature and rainfall during the establishment of the infection, leading to significant genotype-by-environment interactions [START_REF] Campbell | Allocation of Resources: Sources of Variation in Fusarium Head Blight Screening Nurseries[END_REF]Miedaner et al. 2001). Accurate estimation of the level of resistance requires multiple independent phenotyping experiments, replicated over years and/or locations, to avoid confounding effects caused by the environment.

Historically, phenotypic selection has been applied for FHB improvement, evaluating the disease in breeding populations after artificial inoculation at anthesis [START_REF] Bai | Scab of wheat: prospects for control[END_REF].

This approach has yielded cultivars with enhanced resistance but suffers from many drawbacks: it is laborious, time-consuming and costly. More importantly, the development of cultivars combining enhanced FHB resistance with stable grain yield and quality performances remained challenging for breeders [START_REF] Rudd | Host plant resistance genes for Fusarium head blight: sources , mechanisms, and utility in conventional breeding systems[END_REF][START_REF] Bai | Management and resistance in wheat and barley to Fusarium head blight[END_REF].

Since the 1990's and the emergence of molecular markers, QTL (quantitative trait loci) mapping has become the method of choice to dissect the genetic basis of FHB resistance. Due to its worldwide high economic value, most of the QTL mapping projects performed to date have been focusing on common wheat. Buerstmayr et al. (2009) summarized the findings of 52 QTL mapping studies and, among them, only four were performed with tetraploid wheat.

In total, more than 100 FHB-resistance QTL have been identified and 22 genomic regions were detected in at least two common wheat populations. Consistent and reliable QTL were further confirmed by meta-QTL analyses which pointed out 19 confirmed QTL (Liu et al. 2009;Löffler et al. 2009). These QTL are expressed consistently across different genetic backgrounds and environments and are therefore potentially useful for breeders.

The first major resistance QTL for FHB resistance in common wheat was identified from the resistant Asian common wheat cultivar Sumai-3 and mapped to the short arm of the chromosome 3B (Waldron et al. 1999). This QTL, formally designated as Fhb1, is well validated and has been precisely mapped: it is flanked by markers Xgwm533, Xbarc133 and Xgwm493 [START_REF] Cuthbert | Fine mapping Fhb1, a major gene controlling fusarium head blight resistance in bread wheat (Triticum aestivum L.)[END_REF]) and highly diagnostic marker such as Xumn10 are available (Liu et al. 2008;Schweiger et al. 2016). Fhb1 contributes mainly to type 2 resistance and provides some level of type 1 resistance (Anderson et al. 2001;Buerstmayr et al. 2003).

Another well-characterized major QTL derived from Sumai-3 has been mapped on the chromosome 5A (Qfhs.ifa-5A), associated primarily to type 2 resistance [START_REF] Buerstmayr | Molecular mapping of QTLs for Fusarium head blight resistance in spring wheat. I. Resistance to fungal spread (type II resistance)[END_REF]Buerstmayr et al. 2003). Due to their large and stable effect on FHB resistance, these two QTL are promising targets for marker-assisted selection (MAS). Other well-validated and precisely mapped QTL are Fhb2 descending from Sumai-3 and located on the chromosome arm 6BS [START_REF] Cuthbert | Mapping of Fhb2 on chromosome 6BS: A gene controlling Fusarium head blight field resistance in bread wheat (Triticum aestivum L.)[END_REF][START_REF] Dhokane | Integrated Metabolo-Transcriptomics Reveals Fusarium Head Blight Candidate Resistance Genes in Wheat QTL-Fhb2[END_REF] as well as Fhb4 and Fhb5, identified in the Asian common wheat cultivar Wangshuibai and mapped on the chromosome 4B and 5A respectively [START_REF] Xue | Fine mapping Fhb4, a major QTL conditioning resistance to Fusarium infection in bread wheat (Triticum aestivum L.)[END_REF][START_REF] Xue | Precise mapping Fhb5, a major QTL conditioning resistance to Fusarium infection in bread wheat (Triticum aestivum L.)[END_REF].

Although only a few of the many QTL reported for FHB resistance have been validated and deployed in commercial breeding programs, MAS for large effect QTL coupled with phenotypic selection to capture undiscovered small effect QTL is considered to be an efficient strategy for FHB resistance breeding [START_REF] Agostinelli | Optimizing phenotypic and genotypic selection for Fusarium head blight resistance in wheat[END_REF]. Since the last decade, MAS for Fhb1 has been widely implemented in North American common wheat breeding program [START_REF] Anderson | Marker-assisted selection for Fusarium head blight resistance in wheat[END_REF]. MAS can be applied for stacking resistance QTL: FHB resistance is mainly affected by additive effects and pyramiding several QTL using marker-based introgression has been shown to be effective in enhancing FHB resistance and reducing DON contamination in elite common wheat [START_REF] Miedaner | Stacking quantitative trait loci (QTL) for Fusarium head blight resistance from non-adapted sources in an European elite spring wheat background and assessing their effects on deoxynivalenol (DON) content and disease severity[END_REF]. Marker-based backcrossing has also proven efficient to rapidly transfer QTL of exotic resistance sources, such as Sumai-3, into locally adapted backgrounds by avoiding or reducing negative linkage drag. For example, the QTL Fhb1 and Qfhs.ifa-5A were successfully introduced in European elite common wheat background without systematic deleterious yield and quality penalties [START_REF] Der Ohe | Agronomic and quality performance of winter wheat backcross populations carrying non-adapted Fusarium head blight resistance QTL[END_REF][START_REF] Salameh | Effects of introgression of two QTL for fusarium head blight resistance from Asian spring wheat by marker-assisted backcrossing into European winter wheat on fusarium head blight resistance, yield and quality traits[END_REF]. In recent years, several resistant cultivars carrying Fhb1 have been released from North American breeding programs (e.g. [START_REF] Mergoum | Registration of -Faller‖ Spring Wheat[END_REF][START_REF] Anderson | Registration of -Rollag‖ Spring Wheat[END_REF] and in Europe, the variety Jaceo, registered in France in 2012 (Syngenta Seeds), is the first variety carrying Fhb1 commercially available.

In comparison to common wheat, progress for improving FHB resistance in durum wheat has been slow. Durum wheat has been early reported to be more susceptible to FHB than common wheat (Atanasoff 1920;[START_REF] Christensen | Susceptibility of wheat varieties and hybrids to fusarial head blight in Minnesota[END_REF]. Current durum wheat cultivars are generally highly susceptible and the few improved varieties released recently by North American breeding program fail to show levels of resistance equivalent to the ones achieved in common wheat (Zhang et al. 2014). Breeders are still lacking efficient resistance source and research has been targeted at broadening the genetic basis for FHB resistance by introgressing resistance from related species. To date, only resistance from tetraploid wheat has been exploited and, to our best knowledge, durum wheat did not yet benefit from the numerous QTL detected in common wheat. Our work constitutes the first characterization of FHB resistance derived from hexaploid common wheat into elite durum wheat background.

Objectives of the thesis

The main objective of the project was to gain knowledge on the genetics of FHB resistance in durum wheat and to provide breeders with novel germplasm which will support efforts in enhancing durum wheat resistance against FHB.

The first target was to provide a rich source of information on the QTL associated with FHB resistance in tetraploid wheat. I summarized the current status of FHB improvement in durum wheat and provided an overview of the resistance QTL that have been identified for enhancing FHB resistance (Publication 1: Current knowledge on resistance to Fusarium head blight in tetraploid wheat).

The project aimed at broadening the genetic basis for FHB resistance in durum wheat by exploiting resistance source derived from common wheat. I evaluated the effect of the major common wheat resistance QTL Fhb1 in the background of three European elite durum wheat cultivars. The association of FHB resistance with the agronomic traits plant height and flowering date was also examined (Publication 2: QTL mapping of Fusarium head blight resistance in three related durum wheat populations).

Abstract Fusarium head blight (FHB) is a serious threat worldwide due to its dramatic consequences and effects on small grain cereal production such as yield and quality losses and most importantly mycotoxin contamination. Durum wheat (Triticum durum Desf.) is particularly susceptible to FHB. Enhancing resistance has proven difficult due to the narrow genetic variation for this trait in the durum wheat gene pool. Broadening the genetic basis by incorporating resistance alleles from wild and cultivated relatives is a promising approach for durum resistance breeding. This review summarizes the current information on sources available for FHB resistance improvement in durum wheat which include wild and cultivated tetraploid wheat, hexaploid wheat and alien species.

The genetic basis of FHB resistance of a few tetraploid sources in the T. durum background has been dissected by QTL mapping. So far, thirteen QTL with small to moderate effects have repeatedly been detected on 11 chromosomes with alleles improving FHB resistance deriving from relatives and durum wheat itself. Notably, the QTL found in tetraploid wheat populations largely overlap with the QTL identified in hexaploid wheat suggesting a common genetic basis of FHB resistance. FHB resistance breeding by allele introgression into durum wheat is feasible, and QTL pyramiding appears a practicable strategy for durum resistance breeding.

Introduction

Fusarium head blight (FHB) is a persistent threat for wheat growers almost worldwide. A range of Fusarium species has the ability to cause FHB, and their distribution differs depending on agro-ecological conditions. The most pre-eminent species worldwide are Fusarium graminearum Schwabe [teleomorph: Gibberella zeae (Schwein.) Petch], predominant under temperate climate conditions, and Fusarium culmorum (W.G. Smith) Sacc., found more frequently in cooler environments (Parry et al. 1995;[START_REF] Xu | Community ecology of fungal pathogens causing wheat head blight[END_REF]. FHB is responsible for considerable Electronic supplementary material The online version of this article (doi:10.1007/s11032-014-0184-2) contains supplementary material, which is available to authorized users. economic losses in terms of yield drop and quality deterioration of the harvest. The major concern is the contamination of the crop with mycotoxins such as deoxynivalenol (DON), nivalenol and zearalenone. For more background on Fusarium as a cereal pathogen and strategies for disease control refer to Parry et al. (1995), Leonard and Bushnell (2003), [START_REF] Bai | Management and resistance in wheat and barley to Fusarium head blight[END_REF], Buerstmayr et al. (2009), McMullen et al. (2012), Gilbert and Haber (2013).

Mycotoxin contamination of the grains is of particular concern for durum wheat (Triticum durum Desf.) which is used predominantly for semolina and pasta intended for direct human consumption. To ensure food safety, maximum limits for the most prevalent mycotoxins in cereals and cereal products have been established in many countries. The European Commission set a maximum tolerated level of 1.75 ppm for DON in unprocessed durum wheat and of 0.75 ppm in pasta [Commission Regulation (EC) No. 1126[START_REF] Anderson | Marker-assisted selection for Fusarium head blight resistance in wheat[END_REF]. Similarly, the Food and Drug Administration of the USA indicated an advisory level of 1 ppm on finished wheat products for consumption by humans (Guidance for Industry and FDA 2010).

Several factors have deepened the risks of FHB epidemics in wheat. Changes in agricultural practices towards reduced or minimum tillage and a shorter or missing crop rotation between small grains and maize produce a surplus of Fusarium inoculum for subsequent reinfection. Weather patterns characterized by frequent rainfall and high humidity periods promote Fusarium infestations especially around anthesis when wheat is the most susceptible (Osborne and Stein 2007). The growing demand for pasta products has led to an increase in durum wheat production zones. In Europe, the durum wheat growing area has expanded from the traditional Mediterranean basin with warm and dry conditions to more humid regions with climatic conditions conducive for the disease in Central and Western Europe. Cultivation of winter durum, favoured for its higher yield potential, is more likely exposed to Fusarium as its earlier flowering coincides more often with rainfall and wet conditions (Miedaner and Longin 2014). In the upcoming years, durum and bread wheat (Triticum aestivum L.) production is expected to face an increasing pressure of FHB as climate change models forecast a greater risk of contamination associated with a greater prevalence of the highly toxigenic and aggressive F. graminearum (Chakraborty and Newton 2011).

Managing FHB remains difficult, cultural practices and chemical treatment offer only limited efficacy to reduce damages. Breeding resistant cultivars is pivotal and considered the most effective and sustainable strategy to control the disease. While the development of resistant cultivars has been under intensive research in hexaploid bread wheat particularly during the past decade, durum wheat, which is considered a minor crop, has received significantly less attention. Resistant durum wheat cultivars are essentially lacking, and there is an urgent need to identify appropriate resistance sources and understand the genetic basis of FHB resistance in durum wheat. This review aims to summarize the recent advances of breeding for FHB resistance in durum wheat.

Components of FHB resistance and their phenotyping methods

Resistance to FHB in wheat is polygenic and of quantitative nature (Buerstmayr et al. 2009). The complexity of the resistance reaction renders its evaluation and subsequent resistance breeding non-trivial and laborious. Environmental factors significantly influence FHB response by modulating disease infection and development [START_REF] Huhn | Tetraploid Tunisian wheat germplasm as a new source of Fusarium head blight resistance[END_REF]Miedaner and Longin 2014). Accurate evaluations of FHB resistance need to be repeated over environments (years and/or locations). Different phenotypic expressions of the resistance have been described (Schroeder and Christensen 1963;Mesterhazy 1995): Type 1 (resistance to initial infection) and Type 2 (resistance to fungal spread within the spike) are the two components that contribute to ''field resistance'' (Yan et al. 2011) and are usually evaluated in QTL mapping studies.

Different inoculation procedures allow testing for specific resistance components. Single-floret inoculation and measure of speed and/or amount of spread of the symptoms along the ear are typically performed to assess Type 2 resistance. Spray inoculation allows evaluating Type 1 resistance by measuring disease incidence (percentage of ears presenting FHB symptoms). Type 1 resistance is considered difficult to assess, and studies using spray inoculation focus usually on evaluating disease severity (percentage of diseased spikelets per unit area) which encompasses Type 1 and Type 2 resistance (Buerstmayr et al. 2012a). While spray inoculation is considered to mimic natural infection conditions, subsequent FHB evaluations may suffer from environmental effects and are therefore prone to genotype-by-environment interactions (Fuentes et al. 2005;Ma et al. 2006). Most studies performed in tetraploid wheat have relied on evaluating Type 2 resistance which is less biased by environmental variations as the experiments are usually set up in the greenhouse offering bettercontrolled conditions and avoid disease escape because the inoculum is placed directly into the florets.

Further components of resistance have been described notably the resistance to DON accumulation in infected grains also termed Type 3 resistance [START_REF] Miller | Deoxynivalenol and Fusarium head blight resistance in spring cereals[END_REF][START_REF] Mesterhazy | Nature of wheat resistance to Fusarium head blight and the role of deoxynivalenol for breeding[END_REF]. Evaluation of resistance to DON accumulation is done postharvest, and mycotoxin content is usually determined using analytical tools including chromatographic and immunochemical methods (Krska et al. 2008;Berthiller et al. 2013). DON is considered a virulence factor of several Fusarium spp. and has been shown to play a role in the spread of FHB through the spike (Bai et al. 2001). Resistance to toxin accumulation has been demonstrated to play a major role in FHB resistance mechanism in wheat (Lemmens et al. 2005) and, as the other components of resistance, is influenced by environmental conditions (Wegulo 2012;[START_REF] Ovando-Martinez | Analysis of deoxynivalenol and deoxynivalenol-3-glucoside in hard red spring wheat inoculated with Fusarium graminearum[END_REF]. Although reducing DON concentration in grains is a target for breeders, direct selection for Type 3 resistance remains impractical due to its phenotyping costs [START_REF] Sneller | Variation for resistance to kernel infection and toxin accumulation in winter wheat infected with Fusarium graminearum[END_REF].

FHB resistance has frequently been found associated with plant morphological and developmental traits, especially plant height, spike architecture, anther extrusion and flowering date, acting mainly as passive resistance factors (Mesterhazy 1995). The phenotype of a characteristic durum spike differs considerably from the spike of hexaploid bread wheat. The typically compact spike phenotype of durum wheat in combination with the tendency to retain anthers inside the florets may to some extent aggravate disease development.

Genetic resources for improvement of FHB resistance in durum wheat

The generally higher susceptibility of durum wheat in contrast to bread wheat has been noted early on (Atanasoff 1920), and still today, most durum wheat cultivars are susceptible (Clarke et al. 2010;Miedaner and Longin 2014). A prerequisite for resistance breeding is the availability of resistance donors. Unfortunately, variation for this trait is narrow in the species T. durum. Efforts to identify durum wheat accessions with enhanced resistance have met with limited success. [START_REF] Elias | Breeding efforts to develop Fusarium head blight resistant durum wheat in North Dakota[END_REF] screened large collections including several thousand durum wheat accessions and failed to identify resistant lines. A later evaluation of accessions from CIMMYT and ICAR-DIA identified only five Tunisian durum wheat landraces with moderate Type 2 resistance [START_REF] Elias | Breeding efforts to develop Fusarium head blight resistant durum wheat in North Dakota[END_REF][START_REF] Huhn | Tetraploid Tunisian wheat germplasm as a new source of Fusarium head blight resistance[END_REF]. Talas et al. (2011) evaluated Syrian landraces and reported a significant variation for FHB resistance after spray inoculation. The authors identified four accessions with stable resistance as promising candidates for durum wheat breeding.

The reason for the scarcity of FHB-resistant sources in durum wheat has not yet been clearly elucidated. A possible explanation could be that current durum wheat, mostly descending from germplasm cultivated in the warm and summer-dry Mediterranean basin, has not been exposed to relevant disease pressure [START_REF] Ban | CIMMYT's challenges for global communication and germplasm enhancement for FHB resistance[END_REF]. Furthermore, breeding investment in durum wheat has been lower than in bread wheat. As a result, modern durum cultivars are developed by a limited number of durum breeding programs, which may have led to a narrower genetic base compared to hexaploid wheat (Oliver et al. 2008). Several sources suggest that the expression of FHB resistance in durum wheat is compromised by the presence of susceptibility factors and/or suppressor genes in its genome (Stack et al. 2002;[START_REF] Ban | CIMMYT's challenges for global communication and germplasm enhancement for FHB resistance[END_REF][START_REF] Garvin | Quantitative trait locus mapping of increased Fusarium head blight susceptibility associated with a wild emmer wheat chromosome[END_REF][START_REF] Ghavami | Mixed model association mapping for Fusarium head blight resistance in tunisianderived durum wheat populations[END_REF]. To face the lack of resistance sources, breeders have targeted their research at broadening the genetic basis available for durum wheat improvement by searching resistance donors in wild and cultivated relatives.

Hexaploid bread wheat has benefited from intensive research in the last decade, and resistance sources have been identified originating from diverse regions of the world. Among others, the Chinese wheat cultivar Sumai-3 and its derivatives provide among the highest levels of resistance. Major resistance QTL from Sumai-3-derived populations have been consistently identified, namely Fhb1 and Fhb2 on chromosome 3B (Waldron et al. 1999Anderson et al. 2001;Liu et al. 2006) and 6B (Waldron et al. 1999;[START_REF] Shen | Detection of Fusarium head blight resistance QTL in a wheat population using bulked segregant analysis[END_REF][START_REF] Cuthbert | Mapping of Fhb2 on chromosome 6BS: A gene controlling Fusarium head blight field resistance in bread wheat (Triticum aestivum L.)[END_REF], respectively, which contribute to Type 2 resistance, and Qfh.ifa-5A on chromosome 5A [START_REF] Buerstmayr | Molecular mapping of QTLs for Fusarium head blight resistance in spring wheat. I. Resistance to fungal spread (type II resistance)[END_REF](Buerstmayr et al. , 2003a) ) which provides mainly Type 1 resistance and to a lesser extend Type 2 resistance.

Attempts to transfer resistance QTL identified in T. aestivum into T. durum are impeded by differences in ploidy levels and were of limited success so far though some progress has been made. The use of hexaploid wheat as a resistance donor is not straight forward. Even though most of the resistance QTL reported in hexaploid wheat are located on the A and B genome (Buerstmayr et al. 2009), the role of the D-genome, which is absent in tetraploid wheat, may play a role in boosting FHB resistance [START_REF] Fakhfakh | Inheritances of Fusarium head blight resistance in a cross involving local and exotic durum wheat cultivars[END_REF]. Despite that, recent own preliminary results indicate successful transfer of resistance QTL Fhb1 through recurrent back-crossing from Sumai-3 into durum wheat. The introgressed QTL in tetraploid background provides stable and enhanced resistance in field nursery experiments. In contrast, efforts to introgress 5A resistance QTL of Sumai-3 have been hindered by the reduced spike fertility of the durum wheat backcross lines (own unpublished data). To our knowledge, no successful transfer of Fhb2 in tetraploid wheat has been reported.

Resistance that is not confounded by differences in ploidy has been searched in tetraploid relatives of durum wheat. Wild relatives have developed wide genetic adaptation to biotic stresses and offer a large reservoir of genes for durum wheat breeding. Genetic variation in resistance exists in tetraploid wheat subspecies of the primary gene pool of durum wheat. Various studies identified moderately FHB-resistant accessions in wild emmer wheat, T. dicoccoides, cultivated emmer wheat, T. dicoccum, and Persian wheat, T. carthlicum.

The direct progenitor of durum wheat T. dicoccoides has been extensively studied. Miller et al. (1998) screened 290 accessions of T. dicoccoides of the USDA National Small Grains Collections for reaction to FHB and identified several accessions with Type 2 resistance. Buerstmayr et al. (2003b) evaluated 151 lines originating mainly from Israel and pointed out eight accessions with enhanced resistance. A large set of germplasm comprising 416 T. dicoccoides accessions of diverse origins was evaluated by Oliver et al. (2007). The authors noted a broad variation for FHB response with several accessions exhibiting high resistance. Oliver et al. (2008) screened 376 different tetraploid wheat species accessions and successfully identified 16 T. carthlicum and four T. dicoccum with a medium to high level of resistance.

Although these tetraploid species may offer useful sources of resistance for durum wheat improvement, they have received little attention so far in breeding. Up to now, none of the resistant accessions are comparable to Sumai-3 and the use of wild relatives is associated with several difficulties due to their exotic nature that impairs their immediate incorporation in elite breeding programs. To reduce the amount of undesirable linkage drag associated with the introgression of wild alleles, the transfer of resistance from T. dicoccoides accessions to durum wheat has been performed using chromosome substitutions, which yielded experimental lines with increased resistance. Stack et al. (2002) evaluated disomic substitution lines of the moderately resistant T. dicoccoides accession Israel A in the genetic background of the T. durum cultivar Langdon. The line carrying chromosome 3A of T. dicoccoides showed consistently increased FHB resistance. Similarly, substitution lines harbouring chromosome 7A from the T. dicoccoides accession, PI478742, showed consistently enhanced resistance (Kumar et al. 2007).

Recent improvements in chromosome engineering and manipulation permit the incorporation of FHB resistance from more distantly related species of the secondary or tertiary gene pool of durum wheat. Some species from the genera Leymus, Roegneria or Thinopyrum grow in regions with climates favourable to FHB, and some lines have been found with very high to complete resistance [START_REF] Cai | Utilization of alien genes to enhance Fusarium head blight resistance in wheat-a review[END_REF]. They represent a valuable gene pool for FHB improvement.

A FHB resistance locus has been identified on the chromosome 1E of the perennial diploid wild grass Thinopyrum elongatum. Disomic substitution and addition lines of chromosome 1E in the background of T. durum have been successfully developed which express improved resistance (Jauhar 2014). Similarly, another resistance locus from chromosome 7E of T. elongatum has been incorporated in bread wheat using substitution and translocation lines [START_REF] Fu | Molecular cytogenetic characterization of wheat-Thinopyrum elongatum addition, substitution and translocation lines with a novel source of resistance to wheat Fusarium head blight[END_REF]). The method is potentially applicable to durum wheat. The use of alien sources is impeded by their negative agronomic traits, and detailed mapping of the desired locus is underway to efficiently use T. elongatum in FHB resistance improvement [START_REF] Chen | The development of 7E chromosome-specific molecular markers for Thinopyrum elongatum based on SLAF-seq technology[END_REF].

Successful use and incorporation of the resistance loci into adapted cultivars would greatly benefit from precise mapping, to allow targeted QTL selection and at the same time avoid undesired alleles in order to limit unwanted linkage drag.

QTL mapping for FHB resistance in tetraploid wheat

While in hexaploid wheat numerous QTL studies have been performed and more than 100 QTL have been reported (reviewed by Buerstmayr et al. 2009), tetraploid wheat has received less attention. To date, QTL mapping studies have been performed dissecting the genetics of only a few tetraploid resistance sources of T. dicoccoides, T. dicoccum, T. carthlicum and T. durum landraces. We summarize here the QTL reported in crosses with T. durum that have been repeatedly identified in different environments or in independent studies. Details on the mapping population and the inoculation methods performed for each mapping study are presented in Table 1. Information on the relevant QTL detected in tetraploid wheat is given in Table 2. Their estimated positions as well as the position of Fhb1 and Fhb2 hexaploid QTL are indicated by vertical bars on the linkage maps shown in Fig. 1. Linkage maps were drawn with MapChart v2.2 (Voorrips 2002) based on Somers et al. (2004) consensus map available online on GrainGenes database (http://wheat.pw.usda.gov). The map for chromosome 5B relies on the publication by [START_REF] Ghavami | Mixed model association mapping for Fusarium head blight resistance in tunisianderived durum wheat populations[END_REF] as we were not able to anchor the markers provided by the mapping study to the consensus map. For reading ease, only selected markers are displayed in Fig. 1. More detailed information including all available markers with their positions as well as comparison with Marone et al. (2012) consensus map is included in Online Resource 1. The linkage groups shown in Online Resource 1 focus only on the markers located near the QTL. Position of the markers and the genetic distances are kept as in the original consensus maps. Homologous loci used for map comparison are displayed in red. For complete map information, the readers are invited to refer to the original publications.

Most of the studies evaluated Type 2 resistance by single-floret inoculation under greenhouse conditions, and only two studies reviewed herein assessed FHB severity after spray inoculation in field trials. The majority of these mapping studies relied on relatively small population sizes which may impair QTL detection while at the same time tend to over-estimate QTL effects. Primarily, small to moderate effect QTL have been identified on altogether 11 chromosomes, namely 2A, 2B, 3A, 3B, 4A, 4B, 5B, 6A, 6B, 7A and 7B.

Several QTL have been detected in independent studies, such as QTL on chromosomes 2B, 3A, 3B and 6B, which we consider therefore independently validated. The QTL on 3A near Xgwm2 was reported in three unrelated populations using different T. dicoccoides accessions as resistance source (Otto et al. 2002;[START_REF] Gladysz | Evaluation and genetic mapping of resistance to Fusarium head blight in Triticum dicoccoides[END_REF][START_REF] Chen | Saturation and comparative mapping of a major Fusarium head blight resistance QTL in tetraploid wheat[END_REF][START_REF] Buerstmayr | Genetic mapping of QTL for resistance to Fusarium head blight spread (type 2 resistance) in a Triticum dicoccoides × Triticum durum backcross-derived population[END_REF]. The three T. dicoccoides lines are likely to possess the same resistance allele at this locus. Allelic variation for FHB resistance in tetraploid wheat appears for QTL on 6B detected in two mapping populations using T. dicoccum (Buerstmayr et al. 2012b) and T. carthlicum (Somers et al. 2006) accessions as resistant donors. These two diverse tetraploid species probably carry different resistant alleles at the 6B locus.

Most of the QTL regions identified in tetraploid wheat have previously been reported in hexaploid wheat suggesting a common genetic base of resistance. Tetraploid resistance QTL on 2A, 2B, 3A, 3B, 4A, 4B, 6B, 7A, 7B overlap with QTL found in diverse hexaploid-resistant sources comprising spring and winter wheat material of various origins including Asia, Europe and North America [see review by Buerstmayr et al. (2009)]. Notably, QTL on 3B [START_REF] Ghavami | Mixed model association mapping for Fusarium head blight resistance in tunisianderived durum wheat populations[END_REF]Buerstmayr et al. 2012b) and on 6B (Somers et al. 2006;Buerstmayr et al. 2012b) coincide with the major resistance QTL Fhb1 (Liu et al. 2006) and Fhb2 Fig. 1 Location of FHB resistance QTL on durum wheat chromosomes projected on the consensus wheat map by Somers et al. (2004). For readability, only selected markers are shown. Names of the lines contributing the resistant alleles are indicated, and numbers in brackets refer to the publication in which the QTL was reported (for cross reference see Table 1). Approximate QTL positions are designated by vertical bars. Patterns of bars indicate the inoculation method performed [START_REF] Cuthbert | Mapping of Fhb2 on chromosome 6BS: A gene controlling Fusarium head blight field resistance in bread wheat (Triticum aestivum L.)[END_REF], respectively, which both originate from Sumai-3.

Allele comparisons using SSR markers linked to Fhb1 and Fhb2 carried out by Buerstmayr et al. (2012b) revealed different haplotypes for the tetraploid and the hexaploid lines indicating genetic diversity at these loci and different resistance alleles in bread wheat and in tetraploid wheat. The existence of resistance-improving alleles at these loci in tetraploid wheat may eliminate the need to transfer resistance from hexaploid Asian sources into durum wheat.

In hexaploid wheat, Fhb1 has been described to govern the detoxification of DON into the conjugate deoxynivalenol-3-glucoside (DON-3G) (Lemmens et al. 2005). Wheat lines harbouring Fhb1 showed lower FHB symptoms associated with lower amount of total mycotoxins and an increased ability to glycosylate DON, represented by high DON-3G/DON ratio. In durum wheat, variation in response to DON accumulation was recently pointed out. Dall'Asta et al. (2013) detected for the first time the presence of DON-3G in DON contaminated durum wheat samples. Detoxification of DON and accumulation of DON-3G appear also to be a resistance mechanism towards Fusarium infection in durum wheat. Less susceptible lines showed a higher DON-3G/DON ratio and thus an increased DON conversion capacity (Dall'Asta et al. 2013;Cirlini et al. 2014). The genetic basis of DON accumulation resistance in durum wheat has yet to be investigated.

The mapping studies carried out in tetraploid wheat have focused mostly on crosses of T. durum with a resistant relative. Most resistance-improving alleles are derived from the tetraploid wheat relative, but T. durum contributed resistance-improving alleles on 2B (Somers et al. 2006;[START_REF] Gladysz | Evaluation and genetic mapping of resistance to Fusarium head blight in Triticum dicoccoides[END_REF]), 3B [START_REF] Ghavami | Mixed model association mapping for Fusarium head blight resistance in tunisianderived durum wheat populations[END_REF]Buerstmayr et al. 2012b) and 5B [START_REF] Ghavami | Mixed model association mapping for Fusarium head blight resistance in tunisianderived durum wheat populations[END_REF]. Despite its general high susceptibility, durum wheat possesses a certain level of FHB resistance.

Transgressive segregation for FHB resistance was observed when crossing moderately resistant or moderately susceptible lines, and in several mapping populations, a few lines developed lower disease severity than the resistant parent (Somers et al. 2006;[START_REF] Ghavami | Mixed model association mapping for Fusarium head blight resistance in tunisianderived durum wheat populations[END_REF]Ruan et al. 2012). Taking advantage of transgressive segregation is a great opportunity to yield lines with improved resistance. In hexaploid wheat, the cultivar Sumai-3 was selected from a cross of two moderately resistant parents and its outstanding resistance can be explained by a combination of FHB-improving alleles at different loci predominantly acting in an additive manner [START_REF] Bai | Breeding for resistance to Fusarium head blight of wheat in China[END_REF]Schweiger et al. 2013).

Epistatic interactions and the existence of susceptibility factors, which modulate FHB resistance in tetraploid wheat, have been reported. A QTL was found on chromosome 2A of T. dicoccoides that increased FHB susceptibility when transferred into durum wheat. This locus may act as a suppressor of resistance and potentially acts epistatic in reducing the effect of FHB resistance QTL [START_REF] Garvin | Quantitative trait locus mapping of increased Fusarium head blight susceptibility associated with a wild emmer wheat chromosome[END_REF]). [START_REF] Ghavami | Mixed model association mapping for Fusarium head blight resistance in tunisianderived durum wheat populations[END_REF] also suspected the existence of a QTL which mitigates FHB response in the same chromosomal region of 2A in Tunisian durum wheat. Epistatic interactions have also been described by Somers et al. (2006) in a T. durum 9 T. carthlicum population with QTL on 2A and 5A that influenced the FHB resistance QTL on 6B. These findings emphasize the need to select against genetic factors that increase FHB susceptibility or that may suppress resistance.

Of the tetraploid FHB resistance mapping studies performed to date, only two take in consideration morphological and developmental traits in their analyses (Buerstmayr et al. 2012b[START_REF] Buerstmayr | Genetic mapping of QTL for resistance to Fusarium head blight spread (type 2 resistance) in a Triticum dicoccoides × Triticum durum backcross-derived population[END_REF]. It is well accepted that these traits are involved in passive resistance modulating FHB response in wheat. While morphological differences have less impact on disease development in greenhouse experiments using point inoculation, they may have a great effect in field experiments. Thus, considering these plant traits in the analysis of FHB resistance is important.

In the study performed by Buerstmayr et al. (2012b), it appeared that developmental and morphological traits influence FHB severity in tetraploid wheat in the same way as in hexaploid wheat. The large effect resistance QTL on 4B mapped at the position of semi-dwarfing gene Rht-B1 and a QTL on 7B overlapped with QTL for flowering date. Coincidences of resistance QTL with Rht genes are common in hexaploid wheat. It remains unclear whether or not these associations are due to pleiotropic effects, close linkage with resistance genes or mainly an effect of plant height per se. Resistance QTL associated with plant height may have an adverse impact on the agronomic performances of lines and are thus inappropriate for elite breeding programs.

Mapping of QTL underlying important morphological and developmental characteristics needs to be performed upon mapping of resistance QTL as they may have an adverse impact on the agronomic performances of lines. QTL that are not associated with agronomically undesirable traits are to be favoured for efficient improvement of FHB resistance in elite breeding programs. Newly released highdensity consensus maps of durum wheat with larger numbers of markers and providing a better bridge between tetraploid and hexaploid wheat (Maccaferri et al. 2014a, b) will facilitate a more accurate genetic dissection of concurrent QTL effects.

Conclusion

FHB is a serious concern in durum wheat, and there is an urgent need to develop resistant cultivars. The deployment of relatives of durum wheat will enable to expand the genetic diversity for this trait, but their efficient use in elite cultivar breeding is hampered by linkage drag with unfavourable agronomic characteristics. Back-crossing strategies should allow transfer of desired alleles into regionally adapted elite germplasm. Several stable QTL have been detected and genetically mapped. Similarities at the genetic level are observed between tetraploid wheat and hexaploid wheat with most of their resistance QTL overlapping. QTL mapping studies also pointed out that susceptible T. durum possesses some resistance-improving alleles.

Combining resistance alleles through advanced phenotypic selection, marker-assisted selection (MAS) for validated resistance QTL, or genomic selection associated with a selection against suspected susceptibility factors and/or resistance suppressors is a promising approach to enhance FHB resistance in durum wheat breeding programs. Recurrent selection strategies should be employed to rapidly accumulate medium to small effect resistance alleles in breeding populations.

ABSTRACT

Durum wheat (Triticum durum Desf.) is particularly susceptible to Fusarium head blight (FHB) and breeding for resistance is hampered by limited genetic variation within this species.

To date, resistant sources are mainly available in a few wild relative tetraploid wheat accessions. In this study, the effect of the well-known hexaploid wheat (Triticum aestivum L.

KEY MESSAGE

The QTL Fhb1 was successfully introgressed and validated in three durum wheat populations.

The novel germplasm and the QTL detected will support improvement of Fusarium resistance in durum wheat.

KEY WORDS

Tetraploid wheat; durum wheat; Fusarium head blight; resistance breeding; QTL; Fhb1

INTRODUCTION

Fusarium head blight (FHB), caused mainly by Fusarium graminearum and Fusarium culmorum, is one of the major fungal diseases affecting wheat production almost worldwide (Parry et al. 1995). The direct consequences of FHB are yield losses and seed quality reductions in both common wheat (Triticum aestivum) and durum wheat (Triticum durum) (McMullen et al. 2012). Highly problematic is the contamination of infected grains with Fusarium mycotoxins rendering harvests unfit for food and feed (Pestka 2010;Covarelli et al. 2014). Mycotoxin contamination is of particular concern in durum wheat as it is mainly utilized for human consumption. Host plant resistance is considered pivotal for an integrated plant protection strategy to control and reduce FHB damages (Gilbert and Haber 2013).

FHB is a complex disease and its response shows polygenic inheritance modulated by environmental factors with significant genotype-by-environment interactions (Buerstmayr et al. 2009;Löffler et al. 2009). Several components of resistance have been defined (Schroeder and Christensen 1963;Mesterházy 1995) Rht-B1b and Rht-D1b, have been found associated with increased FHB severity under field conditions in common wheat [START_REF] Hilton | Relationship between cultivar height and severity of Fusarium ear blight in wheat[END_REF][START_REF] Miedaner | Effect of Dwarfing Genes on Fusarium Head Blight Resistance in Two Sets of Near-Isogenic Lines of Wheat and Check Cultivars[END_REF][START_REF] Voss | Effect of the Rht-D1 dwarfing locus on Fusarium head blight rating in three segregating populations of winter wheat[END_REF] and in durum wheat (Buerstmayr et al. 2012). Their effect on FHB development may be imputed to plant height per se and differences in canopy structure (Yan et al. 2011) as well as to pleiotropic physiological effects of the Rht genes and/or presence of tightly linked genes [START_REF] Srinivasachary | Semidwarfing Rht-B1 and Rht-D1 loci of wheat differ significantly in their influence on resistance to Fusarium head blight[END_REF][START_REF] Saville | The -Green Revolution‖ dwarfing genes play a role in disease resistance in Triticum aestivum and Hordeum vulgare[END_REF].

Compared to common wheat limited efforts have been dedicated to improve FHB resistance in durum wheat (Buerstmayr et al. 2009). Most current durum wheat cultivars are highly susceptible and breeding progress is hampered by the narrow genetic variation for FHB resistance in durum wheat elite germplasm. Extensive screening of large germplasm collections identified only few durum landraces with improved levels of resistance [START_REF] Elias | Breeding efforts to develop Fusarium head blight resistant durum wheat in North Dakota[END_REF]Talas et al. 2011;[START_REF] Huhn | Tetraploid Tunisian wheat germplasm as a new source of Fusarium head blight resistance[END_REF]. Alternative sources of resistance have been screened in the related tetraploid species of Triticum turgidum to identify resistance donors for breeding (Buerstmayr et al. 2003b;Oliver et al. 2007;Oliver et al. 2008) The QTL detected in tetraploid wheat have failed so far to provide similarly high levels of resistance like Fhb1, the major resistance QTL identified in common wheat cultivar Sumai-3 (Waldron et al. 1999;Anderson et al. 2001). Near diagnostic markers for Fhb1 are available (Liu et al. 2008;Schweiger et al. 2016) and have been successfully implemented into applied wheat breeding using marker assisted selection [START_REF] Anderson | Molecular breeding using a major QTL for fusarium head blight resistance in wheat[END_REF]Wilde et al. 2007;[START_REF] Salameh | Effects of introgression of two QTL for fusarium head blight resistance from Asian spring wheat by marker-assisted backcrossing into European winter wheat on fusarium head blight resistance, yield and quality traits[END_REF]. Notwithstanding, the consequence of transferring this major QTL into tetraploid wheat has not been communicated until now. Here we report on the effect of Fhb1 in three biparental populations that have been generated by crossing line DBC-480, a FHB resistant experimental durum line possessing the Fhb1 allele from Sumai-3, with a modern European durum breeding line and two current durum cultivars. We also show the association of plant height with FHB resistance, and more specifically the effect of Rht-B1 and its interaction with Fhb1 on disease severity in durum wheat.

MATERIALS AND METHODS

Plant materials

Three following good agronomical practice as described in [START_REF] Buerstmayr | Molecular mapping of QTLs for Fusarium head blight resistance in spring wheat. I. Resistance to fungal spread (type II resistance)[END_REF]. At anthesis, trials were spray-inoculated using a motor-driven backpack sprayer in the late afternoons with the virulent DON-producing F. culmorum isolate Fc91015 at a conidial concentration of 2.5 x 10 4 ml -1 . Inoculum suspension was prepared by utilizing the protocol described in Buerstmayr et al. (2000). Aliquots of conidia stock solutions were stored at -30 °C then thawed at 37 °C and diluted with deionized water to achieve the desired final spore concentration just prior to inoculation. Inoculations were performed within each block on all plots, starting when 50% of the plants in the earliest plot of a block reached anthesis. Inoculations were repeated at 2-day intervals and ended two days after the last plot of the block flowered, resulting in up to 6 inoculum applications per block. At each inoculation cycle about 100 ml.m -2 of conidial suspension was sprayed onto the durum wheat heads. The crop canopy was kept moist by mist-irrigating during 20 h after inoculations to facilitate spore germination and infection.

FHB severity was visually estimated as the percentage of infected spikelets within each plot on days 14, 18, 22 and 26 after anthesis. In 2013, scoring was performed at two time points:

18 and 26 days after anthesis. The area under the disease progress curve (AUDPC) was calculated and used as an integrated measure of overall disease severity as described by Buerstmayr et al. (2000). At all experimental plots, plant height (PH) was measured in centimetre and flowering date was recorded and converted into number of days after May 1 st .

The KD population and the respective parental lines Karur and DBC-480 were also tested in the greenhouse for FHB spread within the spike (type 2 resistance) using single-floret inoculation in three unreplicated greenhouse trials at Florimond-Desprez (France) in winter 2015 (GH1) and at IFA-Tulln in summer 2016 (GH2 and GH3). Seeds were germinated in multi-trays and subjected to a cold treatment at 5 °C for one week. Ten seedlings per line were planted in 7.5-liter pots (23.5 cm diameter, 23 cm height) filled with a standard potting mix consisting of 70 % recycled compost, 28 % peat, and 2 % silica sand. Pots were designated as experimental units and arranged in a randomized design. The temperature in the greenhouse was maintained at 22/18 °C (day/night) with a 16-hour photoperiod. Management of the greenhouse trial was essentially as described by [START_REF] Buerstmayr | Genetic mapping of QTL for resistance to Fusarium head blight spread (type 2 resistance) in a Triticum dicoccoides × Triticum durum backcross-derived population[END_REF]. Inoculations were performed at anthesis by pipetting 10 µl of conidia suspension between the lemma and palea of the four outer florets of two central spikelets per spike using the same inoculum preparation and concentration as for the field experiments. High humidity was ensured to promote fungal infection by covering the spikes with translucent polyethylene bags for 24 h. Type 2 resistance was assessed as the percentage of infected spikelets per spike (PIS) measured at 24 days post inoculation by counting the number of infected spikelets and the total number of spikelets per spike. On average, eight spikes per genotype were inoculated in each experiment. Plant height was recorded at each greenhouse pot.

Phenotypic data analysis

Statistical analysis were performed in R 3.1.3 (R development core team, 2016) using the lme4 package for mixed model analysis (Bates et al. 2015). For each trait under investigation, a linear mixed model was fitted for each population with all three experiments combined:

(1) , where is the phenotypic value, µ is the population mean, is the effect of i th genotype, the effect of j th experiment, the effect of the k th replicate within the j th experiment, the ij th effect of the genotype-byexperiment interaction and designated the residual. The genotype effect was treated as fixed and all other terms as random effects. For single experiments a reduced linear mixed model was fitted: (2) , where is the phenotypic value, µ is the population mean, is the effect of i th genotype, the effect of k th replicate (block) and the residual. The genotype effect was again treated as fixed and the replication as random effect.

Fixed and random effects of the models were tested one by one using the likelihood ratio test (LRT). Best linear unbiased estimates (BLUES) of each genotype were computed for the different phenotyped traits according to model (1) for the analysis across experiments and according to model ( 2) for an analysis within individual experiments. BLUES calculated across experiments are also referred to as overall means. Broad sense heritability ( ) was estimated using variance components determined by the restricted maximum likelihood (REML) method setting all effects as random and based on the equation

⁄ ⁄ ⁄
where denotes the genotypic variance, the genotype-by-experiment interaction variance, the error variance, m the number of experiments and p the total number of replications across experiments [START_REF] Holland | Estimating and interpreting heritability for plant breeding: an update[END_REF].

Marker data and genetic map construction

Genomic DNA was extracted from fresh leaves of 10 pooled plants of each line using a simplified CTAB-based procedure modified from Saghai-Maroof et al. (1984). High density genotyping of all individuals was performed using genotyping-by-sequencing (GBS) with the DArTseq platform (DArT PL, Canberra, Australia). Markers identified by the DArTseq assay include SNPs as well as presence-absence variations (PAV) (Li et al. 2015). Markers were filtered based on a reproducibility ≥95%. Furthermore, PAV with ≥10% missing data and SNP markers with ≥10% missing data or heterozygotes were removed for each population separately. Markers showing significant (p<0.01) segregation distortion were also discarded.

Finally, a total of 7965, 4150 and 6235 high quality polymorphic DArTseq markers were available for mapping in the KD, DD and SD populations, respectively. All lines were genotyped with the two selected markers Xbarc147 [START_REF] Song | Development and mapping of microsatellite (SSR) markers in wheat[END_REF] and Xumn10 (Liu et al. 2008) that are known to be linked with Fhb1 as well as with allele-specific markers for Rht-B1 [START_REF] Ellis | -Perfect‖ markers for the Rht-B1b and Rht-D1b dwarfing genes in wheat[END_REF].

Linkage map construction

Linkage maps for each population were constructed using the MSTmap algorithm [START_REF] Wu | Efficient and accurate construction of genetic linkage maps from the minimum spanning tree of a graph[END_REF]) included in the R package ASMap v0.4 [START_REF] Taylor | ASMap: linkage map construction using the MSTmap algorithm[END_REF]. The objective function was set to minimize the sum of recombination events between markers for map construction. In a first step, robust linkage groups where constructed using a p-value threshold set to 1x10 -8 , and the assignment of the linkage groups to chromosome was performed by comparing the location of markers to the wheat DArTseq consensus map provided by DArT PL (A. Kilian, Diversity Arrays Technologies, personal communication, 2016). In a second step, genotypic data were pooled on a chromosome basis and regrouped at a less stringent threshold using a p-value of 1x10 -6 . Distances were calculated with the Kosambi mapping function. Genetic maps were drawn on MapChart software (Voorrips 2002) and collinearity among the individual maps was checked.

QTL mapping

Quantitative trait loci analysis was performed for each trait with the BLUES calculated for each individual experiment and across experiments using the R-package R/qtl (Broman et al. 2003). Missing genotypic information was imputed using the multiple imputation method of [START_REF] Sen | A statistical framework for quantitative trait mapping[END_REF]. Main effect QTL were detected by performing interval mapping and composite interval mapping via Haley-Knott regression. For composite interval mapping the number of marker covariates was selected by a forward approach, while setting a window size of 10 cM. LOD significance threshold for type I error rate α=0.05 were obtained for each trait and experiment based on a 1000 permutations test. Significant QTL were subsequently fitted using a multiple QTL model. The existence of further QTL and the presence of QTL-by-QTL interaction were tested using the addqtl and addint functions, respectively. The final multiple QTL model was fitted against the null model by ANOVA and the percentage of phenotypic variance explained by each QTL, the additive effects as well as LOD scores were estimated.

Confidence intervals were defined for each QTL by calculating a 1.5-LOD support interval.

RESULTS

Trait variations and correlations

Evaluation of FHB severity was performed on three biparental populations in artificially inoculated field trials to investigate the relevant factors that play a role in reducing FHB disease under natural conditions. In all experiments, the common resistant parent DBC-480 was significantly less diseased than the susceptible parents. The average AUDPC value across experiments of the resistant parental line DBC-480 was 125 (corresponding to an average of 12% symptomatic spikelets 26 days after flowering) while Karur, Durobonus and SZD1029K had approximately 5-fold higher AUDPC values (Table 1). Large variation was observed within each population (Fig. 1), but also between populations where the average FHB severity was lowest in the KD population and highest in the SD population. Transgressive segregation was observed in all populations and some lines showed lower disease symptoms than the resistant parent DBC-480, although these differences were not statistically significant. Disease pressure between experiments was comparable in 2013 and 2014 while the experiment of 2015 showed overall higher symptoms. AUDPC broad sense heritability for means across experiments were high and within the same range for the three populations (0.74 < H 2 < 0.89) as in all cases, genotypic variances were higher than variances due to genotype x experiment interaction and residual error (Online Resource 1). Significant genotypic effects for all traits were revealed by ANOVA.

To evaluate specific type 2 component of resistance as conferred by Fhb1, the percentage of infected spikelets per spike (PIS) was measured in three glasshouse experiments for the KD population. Heritability for PIS was moderate H 2 = 0.51 although ANOVA showed significant genotype effects for the 111 RILs (Table 1, Online Resource 1). Some of the RILs showed transgressive segregation for type 2 resistance although only significant for higher susceptibility. As expected, DBC-480 showed less disease symptoms than Karur with an average of 18.3% and 38.4% PIS, respectively (Fig. 1). Weak but significant correlation was observed between means of FHB spread and FHB severity (r = 0.2, p < 0.05).

Variation for plant height was apparent in the three populations (Fig. 1). The susceptible parents Karur, Durobonus and SZD1029K were 38-49 cm shorter than the resistant donor DBC-480. PH showed a bi-modal frequency distribution in the KD and DD populations while a tri-modal distribution was displayed in the SD population (Fig. 1). FHB severity was negatively correlated with PH within all populations (Table 2), accordingly shorter plants showed higher FHB severity. On the contrary, FHB spread after point inoculation (PIS)

showed no significant correlation with PH. Distribution of date of anthesis showed continuous variation in all populations although no significant difference in flowering date was observable among the parents. FHB severity and flowering date were significantly positively correlated in the SD population across experiments, while a weak negative correlation and no evidence for significant correlation were observed in the KD and DD populations, respectively (Table 2).

Within individual experiments however, correlation analysis showed no significant association between disease severity and date of anthesis in 2013 and 2015 for the KD population in 2013 and 2014 for the DD population and in 2014 for the SD population (Online Resource 2).

QTL analysis for FHB spread

QTL detection for FHB spread in the KD population identified a QTL on 3BS which peaked at the SSR marker Xbarc147 and was thus located in the same region as FHB severity 3BS QTL, matching likewise with the Fhb1 locus. The resistance-conferring allele was derived from DBC-480. The QTL was consistently detected in all three individual experiments and for the analysis across all experiments in which it explained 33% of the phenotypic variation (Table 4). Two additional QTL were detected on 2A and 4AL at which the allele of the durum cultivar Karur conferred resistance. These QTL were found in single greenhouse experiments only and, contrary to the QTL at the Fhb1 locus, were not considered as stable.

QTL analysis for plant height and flowering date

QTL for plant height were detected on 4AL, 4BS and 6AS to which DBC-480 alleles contributed to increased height (Table 5). The Rht-B1 locus on 4BS was significant in all populations and explained 95%, 81% and 37% of the variation for PH in the KD, DD and SD population. In the SD population two further QTL were associated with PH on 4AL and 6AS.

The main effects were 11% and 27% for 4AL and 6AS, while epistatic interaction was evident for both loci with the Rht-B1 locus. The percentage of variation explained by the interaction of 4ALx4BS and 6ASx4BS were low compared to the main effects of each locus contributing to 4% and 7% of the phenotypic variance. QTL detection for flowering date revealed significant QTL on 1BL, 2BS, 4AL, 5AL, 6AS and 6BS (Table 5). The DBC-480 allele contributed to a delayed flowering of RILs carrying it on QTL 2BS, 4AL, 5AL, 6AS and 6BS. The QTL on 2BS was found at the same position in all three populations and mapped at a location distal from the QTL for FHB severity identified in the KD population on 2BL. This QTL had the strongest effect in the DD population where it explained 44% of the phenotypic variation. In the SD population, co-localization of QTL for FHB severity, PH and date of anthesis was found on4AL and 6AS and thus these loci appeared to have pleiotropic effects. Quantitative variation for FHB symptoms was evident in all three populations and for both inoculation techniques. FHB severity and FHB spread were significantly but weakly correlated. This low correlation between the two FHB related traits may be explained by the different mechanisms of infection accounted for by the two inoculation methods. FHB severity assessed after spray inoculation in the field accounts for both resistance to primary infection and subsequent spread of the symptoms within the heads. This measure evaluates thus a combination of type 1 and type 2 resistance under conditions that mimic natural epidemics, while single floret inoculation estimates solely type 2 component of resistance. Reports have shown that type 1 and type 2 resistance vary independently among cultivars (Schroeder and Christensen 1963) and are likely controlled by different genes (Buerstmayr et al. 2003a).

Additionally, a high negative correlation between plant height and FHB resistance was evident in the field trials, while no association between these traits was observed in the greenhouse experiments. The discrepancy of plant height influencing FHB response between the two inoculation methods may also contribute to this low correlation as several reports have pointed out type 2 resistance to be less affected by plant height than type 1 resistance (Steiner et al. 2004;Srinivasachary et al. 2008;[START_REF] Srinivasachary | Semidwarfing Rht-B1 and Rht-D1 loci of wheat differ significantly in their influence on resistance to Fusarium head blight[END_REF][START_REF] Lu | Two major resistance quantitative trait loci are required to counteract the increased susceptibility to fusarium head blight of the Rht-D1B dwarfing gene in wheat[END_REF].

Genetic architecture of FHB resistance

The genetic architecture of FHB resistance in our populations appears to be quantitative and oligo-to polygenic. A total of six QTL located on chromosome arms 2BL, 3BS, 4AL, 4BS, 5AL and 6AS were repeatedly associated with enhanced resistance and DBC-480 contributed the favorable alleles at all loci. Genotyping of the populations was performed using GBS DArTseq marker technology supplemented with DNA markers specific to Fhb1 and Rht-B1.

Comparisons of QTL positions were performed based on the consensus wheat map provided by DArT PL (A. Kilian, Diversity Arrays Technologies, personal communication, 2016), which includes DArTseq GBS, DArT and SSR markers, and consensus maps published by Somers et al. (2004) and Marone et al. (2012). It appears that the genomic regions found to be responsible for FHB resistance in our study coincide with locations where QTL have already been identified in common wheat.

The QTL on 3BS mapped at the Fhb1 locus near Xbarc147 and Xumn10 was found repeatedly in all populations. The effect of Fhb1 on FHB severity varied, and depending on the durum genetic background and the individual experiments explained between 5%-16% of the phenotypic variance. In the different populations, the Fhb1 resistance allele reduced FHB severity symptoms on average by 30% in the KD and 36% in the DD populations, while in the SD population the resistance was only increased by 6%. The discrepancies observed among the KD and DD populations on one side, and the SD population on the other side, may be due to differences in their respective resistance genetic architecture. In the KD and DD populations only one further major QTL affecting FHB severity was detected and similar effects for Fhb1 were observed, while in the SD population the relative effect of Fhb1 may be diminished by the presence of three further major QTL. When evaluating FHB spread after single floret inoculation the Fhb1 locus had a large effect explaining 33% of the total phenotypic variance.

Our study demonstrates that in durum wheat Fhb1 is effective in providing type 2 resistance in a similar way as established in common wheat where Fhb1 improves mainly type 2 resistance and to a lesser extent type 1 resistance (Waldron et al. 1999;Anderson et al. 2001;[START_REF] Buerstmayr | Molecular mapping of QTLs for Fusarium head blight resistance in spring wheat. I. Resistance to fungal spread (type II resistance)[END_REF]Buerstmayr et al. 2003a;[START_REF] Cuthbert | Fine mapping Fhb1, a major gene controlling fusarium head blight resistance in bread wheat (Triticum aestivum L.)[END_REF]. Fhb1 is a well characterized QTL descending from the Asian cultivar Sumai-3 which has been found in numerous QTL studies (Buerstmayr et al. 2009). In tetraploid wheat a resistance QTL has also been found in proximity of the Fhb1 genomic region in the durum cultivar Floradur (Buerstmayr et al., 2012) and in Tunisian durum landraces [START_REF] Ghavami | Mixed model association mapping for Fusarium head blight resistance in tunisianderived durum wheat populations[END_REF]. However, haplotype comparison using SSR markers by Buerstmayr et al. (2012) revealed different alleles for Sumai-3 and Floradur at the Fhb1 locus indicating thus the existence of different QTL alleles at this locus.

We report here the first successful deployment of Fhb1 in durum wheat which marks a significant step forward in durum wheat breeding towards improving FHB resistance.

Common wheat represents a useful reservoir of resistance for durum wheat as most of the QTL that have been identified are located on the A and B genomes (Buerstmayr et al. 2009;Liu et al. 2009;Löffler et al. 2009). The difficulties pointed out in previous studies when transferring resistance QTL from common wheat into durum wheat may be attributed to complex interactions of genes among the A, B and D genomes as emphasized in a recent study by Zhu et al. (2016a). In our study no epistatic interactions that may modulate the effect of Fhb1 were detected. The absence of the D genome in durum wheat, hypothesized to carry factors that enhance resistance [START_REF] Fakhfakh | Inheritances of Fusarium head blight resistance in a cross involving local and exotic durum wheat cultivars[END_REF], has been speculated one of the limiting factors for effective deployment of resistance from hexaploid wheat. Our results show that the presence of the D genome appears to be not required for efficient expression of Fhb1 in durum wheat. Comparing the effect of Fhb1 in durum wheat with previous studies is not trivial due to wide range of phenotypic variances reported for this QTL in common wheat (Buerstmayr et al. 2009). In studies evaluating type 2 resistance in common wheat, R² values for Fhb1 ranged between 11% (Yang et al. 2005) and 60% [START_REF] Bai | Amplified fragment length polymorphism markers linked to a major quantitative trait locus controlling scab resistance in wheat[END_REF] while in spray inoculated field trials Buerstmayr et al. (2003a) reported an R² of 29%. The resistance improving effect of Fhb1 in our durum wheat populations is in a similar range as reported in a series of near isogenic lines in common wheat by [START_REF] Pumphrey | Validating the Fhb1 QTL for fusarium head blight resistance in near-isogenic wheat lines developed from breeding populations[END_REF] who found an average reduction of disease severity by 23%, though varying from 0 to 70%. Differences in population size, genetic background, inoculation techniques and environments in which the evaluations were performed can all be reasons for these variations. While in the literature, there are speculations that durum wheat may carry or lack certain genetic factors that modulate the resistance improving effect of Fhb1 [START_REF] Rudd | Host plant resistance genes for Fusarium head blight: sources , mechanisms, and utility in conventional breeding systems[END_REF], we find no evidence to support this hypothesis.

A major QTL on 4BS associated with FHB severity was found in all three populations with effects of different magnitude. The location of the QTL coincided with the Rht-B1 gene. The QTL was responsible for the greatest amount of variation for resistance in the KD and DD populations while in the SD population the QTL had a major effect but was not the greatest contributor to FHB resistance. As mentioned previously, the discrepancy of effects observed is certainly due to differences in genetic backgrounds. In all cases, the reduced height allele Rht-B1b accounted to higher disease severity. Such associations of the semi-dwarf Rht-B1b allele with increased FHB severity have been previously reported in hexaploid wheat [START_REF] Hilton | Relationship between cultivar height and severity of Fusarium ear blight in wheat[END_REF][START_REF] Srinivasachary | Semidwarfing Rht-B1 and Rht-D1 loci of wheat differ significantly in their influence on resistance to Fusarium head blight[END_REF]). Supporting results have also been found in three durum wheat backcross populations from crosses of the tall and FHB resistant donor T. dicoccum-line 161 to the semi-dwarf durum wheat lines Helidur, Floradur and DS-131621. The resistance QTL at the Rht-B1 locus was the most important QTL affecting FHB resistance after spray inoculation and in all three populations, plants carrying the Rht-B1b allele showed higher FHB severity scores (Buerstmayr et al. 2012).

In the SD population two further major QTL were detected on 4AL and 6AS. Both resistance QTL overlapped with QTL for flowering date and plant height. QTL have been already identified on 4A and 6A in tetraploid wheat, however they appear to be located on different chromosome arms and do not match the position of the QTL identified in our study. [START_REF] Gladysz | Evaluation and genetic mapping of resistance to Fusarium head blight in Triticum dicoccoides[END_REF] identified a QTL for type 2 resistance derived from the resistant T. dicoccoides accession Mt.Hermon#22 near Xgwm610 which mapped on the short arm of chromosome 4A while Buerstmayr et al. (2012) found a small effect QTL for FHB severity derived from T.dicoccum-line 161 in a cross with line DS-131621 near Xgwm356 on 6AL. Meanwhile, several mapping projects performed in hexaploid wheat identified QTL in the same region of 4AL in the U.S winter wheat Heyne [START_REF] Zhang | Quantitative trait loci for Fusarium head blight resistance in U.S. hard winter wheat cultivar Heyne[END_REF]) and in the Swiss winter wheat Arina [START_REF] Paillard | QTL analysis of resistance to Fusarium head blight in Swiss winter wheat (Triticum aestivum L.)[END_REF][START_REF] Buerstmayr | Comparative mapping of quantitative trait loci for Fusarium head blight resistance and anther retention in the winter wheat population Capo × Arina[END_REF]. No coinciding QTL for flowering date or plant height were reported but an overlap with QTL for anther retention was found in the Arina/Capo population [START_REF] Buerstmayr | Comparative mapping of quantitative trait loci for Fusarium head blight resistance and anther retention in the winter wheat population Capo × Arina[END_REF]. The QTL on 6AS mapped to a similar position as the type 2 resistance QTL identified in hexaploid wheat in the ND2603/Butte86 population derived from the resistant line ND2603 (Sumai 3/Wheaton) (Anderson et al. 2001).

In the KD population a minor effect QTL was found on 2BL at the proximity of the centromere. This region has been reported to carry resistance QTL in two unrelated tetraploid wheat populations where the susceptible durum wheat parents Strongfield (Somers et al. 2006) and Helidur [START_REF] Gladysz | Evaluation and genetic mapping of resistance to Fusarium head blight in Triticum dicoccoides[END_REF]) contributed the resistance improving allele. These QTL were detected after point inoculation providing type 2 resistance while the QTL identified in our study was found after spray inoculation.

Another QTL for FHB severity was identified on 5AL in the DD population, which had a major effect in 2013 but remained undetected in 2014 and 2015. In the DD population very few GBS markers were polymorphic on chromosome 5A making exact positioning of the QTL difficult. In order to improve map density 21 SSR markers were additionally screened, yet none was found to be polymorphic suggesting close genetic relatedness of the parental lines for this genomic region. Comparison with previous studies is therefore difficult but map comparison suggests that the QTL does not map to the same region as the major hexaploid wheat QTL on 5A Qfhs.ifa-5A derived from Sumai-3 which is located close to the centromere (Buerstmayr et al. 2003a).

Association of QTL for FHB resistance, flowering date and plant height

In our study 6 QTL were found associated with flowering date. Co-localization of QTL for flowering date and FHB resistance was evident for the SD population on 4AL and 6AS. The two QTL exert a strong effect on both traits for which a positive correlation was observed. In the KD and DD populations weak and non-significant correlations were found, and when individual experiments were analyzed separately, the correlations varied greatly. No general pattern was evident for the association between earliness and the level of FHB symptoms in these two populations. This non-dependency may be attributed to the absence of overlapping QTL for these two traits, while environment-specific factors around flowering and inoculation may account for variability in the correlations observed in individual experiments.

In contrast, plant height was significantly negatively correlated with FHB severity in all three populations, which is in agreement with previous findings (Talas et al. 2011;Buerstmayr et al. 2012;Miedaner and Longin 2014). All PH QTL identified in this study coincided with QTL for FHB severity on chromosomes 4AL, 4BS and 6AS. Co-localization of PH and FHB severity QTL is a common feature in wheat and supported by meta-QTL analysis [START_REF] Mao | Confirmation of the relationship between plant height and Fusarium head blight resistance in wheat (Triticum aestivum L.) by QTL metaanalysis[END_REF]. The mechanisms of association between the two traits are complex and may be attributed to effects of height differences per se and/or to pleiotropic effects of the dwarfing genes or tightly linked genes that increase FHB susceptibility. The mutant allele Rht-B1b, as well as its homoeologous allele Rht-D1b on chromosome 4D, encode single nucleotide polymorphism (SNP) mutations in the DELLA domain that create a premature stop codon that is responsible for reduced sensitivity to the phytohormone gibberellin leading to shorter plant height (Peng et al. 1999;Hedden and Sponsel 2015). DELLA proteins have been shown to be associated with abiotic and biotic stress tolerance [START_REF] Achard | Releasing the brakes of plant growth: How GAs shutdown DELLA proteins[END_REF] and in the case of FHB, a DELLA protein mutation may have physiological effects linked to changes in cell death response [START_REF] Saville | The -Green Revolution‖ dwarfing genes play a role in disease resistance in Triticum aestivum and Hordeum vulgare[END_REF]. Alternatively to these genetic effects, differences in microclimatic conditions around the heads of tall and dwarf genotypes have been considered to play a significant role particularly under field conditions, with short plants being exposed to higher infection pressure than tall plants (Yan et al. 2011). The Rht-B1b allele is also known to have pleiotropic effects on different morphological and structural traits including reduced peduncle length and increased cell density which may also affect response to FHB. In common wheat Rht-B1b and Rht-D1b were found associated with reduced anther extrusion, which was supposed to partly explain their association with higher FHB susceptibility (Buerstmayr and Buerstmayr 2016). In the case of our study, all features may be important.

The strong effect of the QTL on 4BS, coinciding with the reduced height gene Rht-B1, on PH and FHB severity was evident in all populations. The Rht-B1 locus explained 95%, 81% and 37% of the variation for PH and 64%, 38% and 19% of the variation for FHB severity in the KD, DD and SD populations, respectively. In the SD population the two additional QTL on 4AL and 6AS exerted at the same time strong effect on plant height and FHB resistance. The QTL on 4AL mapped to a similar region as a QTL associated with PH in hexaploid wheat corresponding to a kaurenic acid oxidase (KAO) gene (Khlestkina et al. 2010;Zanke et al. 2014), while reduced height genes have been reported on 6AS in durum wheat (Haque et al. 2011). These genes are gibberellin-sensitive and not comparable to Rht-B1 in that aspect. In agreement with Yan et al. (2011), we hypothesize that considering the large variation for plant height with differences of about 60 cm between the shortest and the tallest plants, part of the apparent negative correlation may be attributed to plant height per se. Even under sprayinoculation and mist-irrigation, heads of short plants tend to remain more humid and therefore under more severe infection pressure than heads of tall plants. This is in agreement with Buerstmayr et al. (2012) who evaluated FHB severity of three durum wheat populations with similarly large variation for plant height as observed in our present study and argued for a probable disease escape of tall lines despite controlled mist-irrigation after spray-inoculation.

Perspective for durum wheat breeding and conclusion

Obviously in our populations plant height had a strong influence on modulating FHB disease response. The increased FHB susceptibility associated with medium to short height plant and with Rht-B1b is challenging for durum wheat breeders. Rht-B1b confers beneficial attributes linked to higher yield and harvest index concomitant to the desired reduced plant height, thereby limiting lodging, in plant production systems with modern agronomic practices (Royo et al. 2007;Subira et al. 2016). We show that the successful deployment of Fhb1 in combination with minor effect QTL enabled the discovery and the selection of semi-dwarf lines with upsurge levels of resistance. These results are in agreement with a previous report in hexaploid wheat where pyramiding two resistance QTL balanced the negative effect of the semi-dwarf allele Rht-D1b to achieve improved levels of resistance in semi-dwarf wheat [START_REF] Lu | Two major resistance quantitative trait loci are required to counteract the increased susceptibility to fusarium head blight of the Rht-D1B dwarfing gene in wheat[END_REF]. The progeny lines of the KD and DD populations carrying favorable allele combinations at the Rht-B1 and Fhb1 loci, and additional FHB resistance alleles on 2BL or 5AL provide unique and novel resources for durum wheat breeding. The introgression of Fhb1 by recurrent backcrossing into durum wheat to develop the resistant experimental line DBC-480 and its crossing to elite durum cultivars enabled the development of novel FHB resistant breeding lines that are agronomically close to modern European germplasm. These novel improved lines are thus readily incorporable into practical durum wheat breeding programs for enhancing FHB resistance. Only a limited number of QTL mapping have been performed so far to dissect the genetic basis of resistance in tetraploid wheat and have widely relied on the use of wild and cultivated relative resistant sources. Stable QTL of small to moderate effect have been identified and, most interestingly for durum wheat breeders, resistance-conferring QTL have been also

detected in the susceptible durum wheat cultivars. A persistent finding of QTL mapping investigations is that most of the QTL identified in tetraploid wheat coincide with QTL detected in common wheat, thereby suggesting similarities at the genetic level for FHB resistance.

The aim of this work was to evaluate and validate for the first time the effect of Fhb1 -from the Asian common wheat Sumai-3in durum wheat background. The transfer of resistance from common wheat to durum wheat is obviously not straightforward as no successful deployment had been reported until now. Recurrent backcrossing of Sumai-3 into durum wheat and thorough phenotypic selection allowed the identification of the improved tetraploid experimental lines DBC-480 carrying an Fhb1 introgression. DBC-480 was crossed with three elite durum wheat cultivars and Fhb1 was detected in all three mapping populations, explaining between 5%-16% of the phenotypic variance for FHB severity depending on the genetic background. Plant height heavily influenced FHB resistance in these populations, and the semi-dwarf allele Rht-B1b was associated with increased FHB severity. Nonetheless, the negative effect of Rht-B1b on FHB resistance was largely compensated in lines carrying also

Fhb1. Lines with moderate height and enhanced levels of resistance have been selected and provide new resources for breeding durum wheat cultivars with improved resistance.

The use of non-adapted resistance donors in breeding programs may be hindered by the presence of linkage drag associated with deleterious agronomic characteristics or negative quality traits. The lines developed in our study are agronomically close to modern durum wheat germplasm, representing a great asset for their implementation in breeding programs.

In durum wheat the genetic architecture of FHB resistance shows mainly additive inheritance, although some epistatic interactions and the presence of genetic factors that increase susceptibility have been reported in previous studies. The use of MAS, for pyramiding resistance QTL and recurrent selection approach appear promising for rapidly developing durum wheat cultivars with enhanced FHB resistance. markers can be obtained from the original publications. Names of the lines contributing the resistant alleles are mentioned and numbers in brackets refer to the publication in which the QTL was reported (for cross reference see Table 1).

Homologous loci between the maps of the same chromosome are colored in red.

Résumé

Caractérisation des déterminants génétiques de la résistance à la fusariose chez le blé dur

Importance économique du blé dur

Le blé est une des principales denrées alimentaires dans le monde, représentant environ 20% des apports caloriques totaux consommés par les humains. Le blé est la première céréale en termes de surfaces agricoles cultivées, devançant le riz et le maïs, avec une production mondiale atteignant en 2015 plus de 730 millions de tonnes (International Grains Council). La culture de blé englobe différentes espèces parmi lesquelles le blé tendre hexaploïde (Triticum aestivum L.) qui en constitue la quasi-totalité et qui représente plus de 90% du blé cultivé à travers le monde. Le blé dur tétraploïde (Triticum durum Desf.), avec un total de 39 millions de tonnes produites en 2015, représente quant à lui, environ 5% de la production globale de blé. Le blé dur est considéré comme une culture secondaire à l'échelle mondiale. Il est toutefois la culture principale et la denrée alimentaire de base du bassin méditerranéen où il est cultivé traditionnellement. Le blé dur est presque exclusivement utilisé pour l'alimentation humaine et constitue, de fait, une culture d'importance économique majeure. La qualité du grain est un aspect important pour la transformation du blé dur. La qualité du grain inclut une teneur élevée en pigments jaunes et en protéines, une bonne qualité du gluten, la vitrosité et une faible proportion de grains malades (Troccoli et al. 2000). Sur le marché mondial, les grains de haute qualité sont recherchés pour la fabrication de pâtes de qualité supérieure. Le blé dur est également consommé sous la forme de coucous, de boulgour et de pain plats (Elias 1995).

La fusariose de l'épi

La fusariose de l'épi est une des principales maladies fongiques qui affectent la production de blé à travers le monde (Parry et al. 1995). La fusariose est responsable non seulement de pertes économiques directes dues à des baisses de rendements et de qualité des grains infectés mais également responsable de pertes indirectes en affectant la qualité sanitaire des récoltes en raison de la présence de mycotoxines dans les grains. Cette maladie est provoquée par un complexe de champignons pathogènes, du genre Fusarium et Microdochium, qui regroupe plus de 19 espèces capables d'induire la fusariose. La fréquence à laquelle ces espèces sont retrouvées dépend à la fois de la localisation géographique et des conditions climatiques locales, principalement la température et l'humidité (Xu et al. 2005;[START_REF] Xu | Relationship between the fungal complex causing Fusarium head blight of wheat and environmental conditions[END_REF]. Fusarium graminearum [téléomorphe:

Gibberella zeae], prédomine généralement sous des conditions humides et chaudes et est l'espèce la plus importante en Amérique du Nord, en Europe Centrale et en Australie, alors que Fusarium culmorum [téléomorphe inconnu] est retrouvé plus fréquemment en Europe de l'Ouest (Parry et al. 1995). Parmi les différents agents causant la fusariose, ces deux espèces sont hautement pathogènes et leurs isolats sont tous susceptibles de produire des métabolites secondaires toxiques, notamment le déoxynivalénol (DON), qui s'accumulent dans les grains infectés. Du fait de leur importance sur l'incidence de la maladie, F. graminearum et F. culmorum, sont principalement utilisés par les sélectionneurs et les chercheurs lors des essais par inoculations artificielles, avec toutefois la majorité des études épidémiologiques se concentrant sur F. graminearum uniquement.

Le blé est particulièrement sensible à la maladie lors de la floraison. L'infection peut avoir lieu tout au long du développement du grain jusqu'au stade de grain pâteux. Les épidémies de fusariose sont favorisées par une humidité élevée et des précipitations importantes au cours du printemps. Le risque d'infestation est d'autant plus élevé qu'on se retrouve face à une forte présence d'inoculum naturel. Les agents pathogènes de la fusariose sont non-hôtes spécifiques et peuvent contaminer un grand nombre de plantes, notamment les céréales comme le blé tendre, le blé dur, le triticale, le seigle ou le maïs (Parry et al. 1995;[START_REF] Inch | The incidence of Fusarium species recovered from inflorescences of wild grasses in southern Manitoba[END_REF]. Les symptômes de la maladie apparaissent quelques jours après l'infection, caractérisés par des liaisons nécrotiques sur l'extérieur de la surface des glumes et l'apparition d'épillets prématurément échaudés. Plusieurs épillets d'un même épi peuvent être affectés, la maladie pouvant progresser jusqu'à l'échaudage complet de l'épi. Au sein des épillets infectés, les grains peuvent être absents ou présenter un aspect atrophié entrainant une baisse de rendement liés à une réduction du nombre de grains et du poids spécifique (Parry et al. 1995 ;[START_REF] Bushnell | Histology and Physiology of Fusarium Head Blight[END_REF]. La contamination des grains en développement peut également être associée à l'accumulation de mycotoxines. Les grains fusariés (« Fusarium-diseased kernels » ou FDK) ont une apparence typique : mince, ridée et rugueuse, de couleur blanchâtre à brunâtre. Les grains contaminés plus tardivement peuvent présenter une apparence normale bien que contenant des mycotoxines [START_REF] Cowger | Post-anthesis moisture increased Fusarium head blight and deoxynivalenol levels in North Carolina winter wheat[END_REF]Siou et al. 2014).

Les dommages causés par la fusariose de l'épi sont multiples. Lors de fortes épidémies, les rendements peuvent être considérablement réduits et les lots contenant des grains fusariés susceptibles d'être déclassés ou éliminés (McMullen et al. 1997). La maladie a des effets néfastes sur les propriétés de la mouture et de la fabrication des pâtes du fait de la détérioration de la teneur en protéines et de la force du gluten des grains fusariés (Dexter et al. 1996;Nightingale et al. 1999).La principale préoccupation associée à la fusariose est la présence de mycotoxines dont l'exposition, par ingestion de grains infectés, provoque de graves mycotoxicoses représentant un L'adoption de pratiques culturales sans labour ou avec labours restreints, alliées à la présence de plantes hôtes sensibles, telles que le maïs, dans les rotations culturales, favorise le développement de l'inoculum primaire, augmentant ainsi les risques d'infections pour la culture suivante (Mc Mullen et al. 1997). Les conditions climatiques caractérisées par des pluies fréquentes et une forte hygrométrie autour de la période de floraison du blé, sont favorables à l'initiation et au développement de la fusariose (Osborne and Stein 2007). La demande croissante en pâtes alimentaires a engendré une expansion de la zone de culture du blé dur vers des régions où les conditions climatiques sont propices au développement de la maladie. En Europe, la production de blé dur s'est étendue des régions chaudes et sèches du pourtour Méditerranéen vers des régions plus humides d'Europe centrale et occidentale. La culture de blé dur d'hiver, possédant un potentiel de rendement plus élevé, est également d'avantage exposée à un risque d'infection du fait de sa date de floraison plus précoce coïncidant souvent avec une hygrométrie élevée (Miedaner and Longin 2014).

La résistance à la fusariose

L'utilisation de variétés résistantes est considérée comme essentielle en matière de lutte intégrée contre la fusariose et comme le levier le plus efficace et le plus économique pour contrôler et réduire les dommages liés à la maladie (Gilbert and Haber 2013). La résistance à la fusariose est de nature quantitative et polygénique, contrôlée par de nombreux loci à caractères quantitatifs (QTL ou « quantitative trait loci »). L'expression de la résistance à la fusariose est modulée par les facteurs environnementaux, en particulier la température et l'hygrométrie lors de l'établissement de l'infection, impliquant des interactions génotype x environnement [START_REF] Campbell | Allocation of Resources: Sources of Variation in Fusarium Head Blight Screening Nurseries[END_REF]Miedaner et al. 2001). L'estimation précise du niveau de résistance requiert donc une évaluation au sein d'essais indépendants, répétés sur plusieurs années et/ou plusieurs lieux, afin de réduire la variabilité associée aux facteurs environnementaux.

Plusieurs types de résistance à la fusariose ont été décrits et sont communément acceptés et étudiés lors des analyses de QTL de résistance (Schroeder and Christensen 1963;Mesterhazy 1995) parmi lesquels la résistance à l'infection initiale (pénétration), dite de type 1, ainsi que la résistance à la propagation du pathogène dans l'épi, dite de type 2. Des procédures d'inoculations spécifiques permettent d'évaluer ces différents types de résistance. La résistance de type 2 est généralement estimée après inoculation ponctuelle en évaluant la vitesse de progression des symptômes ou le nombre d'épillets infectés le long de l'épi. L'inoculation par spray permet d'évaluer la résistance de type 1 en mesurant l'incidence de la maladie (nombre d'épis présentant des symptômes). L'évaluation de la résistance de type 1 est difficile à réaliser et de fait, les essais utilisant l'inoculation par spray mesurent le plus souvent la sévérité de la maladie (pourcentage d'épillets infectés par unité de surface) qui englobe les résistances de type 1 et 2 (Buerstmayr et al. 2012a).

En parallèle des mécanismes actifs de résistance, des mécanismes dits passifs modulent également la réponse à la fusariose (Mesterhazy 1995). Ces mécanismes incluent des caractéristiques morphologiques ou développementales qui affectent notamment la capacité du pathogène à pénétrer dans l'épi et le développement de la maladie par des phénomènes d'évitement. La taille des plantes est considérée comme un des facteurs morphologiques le plus important lié à la résistance à la fusariose. Les allèles de nanismes, Rht-B1b et Rht-D1b, sont associés à une plus grande sensibilité à la maladie chez le blé dur tétraploïde (Buerstmayr et al. 2012b) et le blé tendre hexaploïde [START_REF] Hilton | Relationship between cultivar height and severity of Fusarium ear blight in wheat[END_REF][START_REF] Miedaner | Effect of Dwarfing Genes on Fusarium Head Blight Resistance in Two Sets of Near-Isogenic Lines of Wheat and Check Cultivars[END_REF][START_REF] Voss | Effect of the Rht-D1 dwarfing locus on Fusarium head blight rating in three segregating populations of winter wheat[END_REF]. Cet effet sur la résistance à la fusariose peut être expliqué par la hauteur des plantes per se et par les différences de structure de canopée favorisant le développement du pathogène (Yan et al. 2011), aussi bien que par des effets pléiotropiques des gènes Rht et/ou par la présence de gènes liés [START_REF] Srinivasachary | Semidwarfing Rht-B1 and Rht-D1 loci of wheat differ significantly in their influence on resistance to Fusarium head blight[END_REF][START_REF] Saville | The -Green Revolution‖ dwarfing genes play a role in disease resistance in Triticum aestivum and Hordeum vulgare[END_REF].

Plus d'une centaine de QTL de résistance à la fusariose chez le blé tendre ont été décrits dans la littérature (Buerstmayr et al. 2009;Liu et al. 2009;Löffler et al. 2009). Le premier QTL à effet majeur à avoir été identifié chez le blé tendre provient de la variété asiatique Sumai-3 et est localisé sur le bras court du chromosome 3B (Waldron et al. 1999). Ce QTL, appelé Fhb1, est particulièrement bien validé et utilisé comme source de résistance dans les programmes de sélection. Fhb1 est précisément cartographié. Il est flanqué par les marqueurs Xgwm533, Xbarc133 and Xgwm493 [START_REF] Cuthbert | Fine mapping Fhb1, a major gene controlling fusarium head blight resistance in bread wheat (Triticum aestivum L.)[END_REF]) et des marqueurs diagnostics tels que Xumn10 sont disponibles (Liu et al. 2008;Schweiger et al. 2016). Fhb1contribue principalement à la résistance de type 2 et, dans un moindre mesure, à la résistance de type 1 (Anderson et al. 2001;Buerstmayr et al. 2003a).

La plupart des études de détection de QTL de résistance à la fusariose ont été menées chez le blé tendre du fait de son importance économique au niveau mondial. Parmi les 52 analyses de QTL répertoriées par Buerstmayr et al. (2009), seules quatre ont été réalisées sur le blé tétraploïde. Les efforts consacrés à l'amélioration de la résistance du blé dur à la fusariose sont limités et les progrès, en comparaison avec le blé tendre, sont lents.

Dans une première partie de la thèse, les ressources génétiques disponibles pour l'amélioration de la résistance à la fusariose ainsi que les QTL détectés à ce jour chez le blé tétraploïde ont été résumées. Ce travail a fait l'objet d'une publication dans le journal Molecular Breeding sous la forme d'une revue scientifique [START_REF] Prat | Current knowledge on resistance to Fusarium head blight in tetraploid wheat[END_REF].

Ressources génétiques pour l'amélioration de la résistance à la fusariose chez le blé dur

Le blé dur a depuis longtemps été signalé comme plus sensible à la fusariose que le blé tendre (Atanasoff 1920;[START_REF] Christensen | Susceptibility of wheat varieties and hybrids to fusarial head blight in Minnesota[END_REF]. La plupart des cultivars de blé dur actuels présentent une haute sensibilité à la maladie. Les quelques variétés avec un niveau de résistance amélioré, issues des programmes de sélection Nord-Américains, ne présentent pas des niveaux de résistance équivalents à ceux atteints chez le blé tendre (Zhang et al. 2014). Jusqu'à présent, les progrès pour améliorer la résistance à la fusariose ont été freinés par la faible variation génétique disponible pour ce caractère au sein du germoplasme de blé dur. Le criblage d'importantes collections n'a permis l'identification que de seulement quelques variétés locales, ou landraces, avec un meilleur niveau de résistance à la fusariose [START_REF] Elias | Breeding efforts to develop Fusarium head blight resistant durum wheat in North Dakota[END_REF]Talas et al. 2011;[START_REF] Huhn | Tetraploid Tunisian wheat germplasm as a new source of Fusarium head blight resistance[END_REF].

La raison pour laquelle il existe peu de sources de résistance à la fusariose chez le blé dur n'a pas encore clairement été élucidée. Une des explications avancée indique que les cultivars de blé dur actuels, issus principalement de germoplasme cultivé dans les conditions chaudes et sèches du bassin méditerranéen, n'aurait pas été exposés à des conditions de fortes pressions de la maladie [START_REF] Ban | CIMMYT's challenges for global communication and germplasm enhancement for FHB resistance[END_REF]. En outre, les investissements dans les programmes de sélection de blé dur ont été plus faibles comparé au blé tendre. Par conséquence, les variétés modernes de blé dur ont été développées à partir d'un nombre restreint de programmes de sélection, ce qui a pu mener à une base génétique plus étroite par rapport au blé tendre (Oliver et al. 2008). Enfin, différents auteurs ont suggéré l'existence de facteurs de sensibilité et/ou la présence de gènes suppresseurs dans le génome du blé dur qui affaiblirait sa résistance à la fusariose (Stack et al. 2002;[START_REF] Ban | CIMMYT's challenges for global communication and germplasm enhancement for FHB resistance[END_REF][START_REF] Garvin | Quantitative trait locus mapping of increased Fusarium head blight susceptibility associated with a wild emmer wheat chromosome[END_REF][START_REF] Ghavami | Mixed model association mapping for Fusarium head blight resistance in tunisianderived durum wheat populations[END_REF]. Pour faire face à ce déficit de sources de résistance, les sélectionneurs ont ciblé leurs recherches vers le criblage de matériel résistant au sein d'espèces apparentées, sauvages et cultivées, afin d'élargir la base génétique utilisable pour l'amélioration de la résistance du blé dur à la fusariose.

Le blé tendre hexaploïde a bénéficié d'intenses efforts de recherche ce qui a permis l'identification de sources de résistances issues de diverses régions du monde. Parmi celles-ci, la variété de blé tendre chinois Sumai-3 confère un des plus hauts niveaux de résistance. Les tentatives de transfert de QTL de résistance identifié chez le blé tendre hexaploïde vers le blé dur tétraploïde sont gênées par les différences de niveau de ploïdie et ont eu, jusque-là, un succès limité. L'utilisation du blé tendre comme source de résistance pour le blé dur n'est pas simple.

Bien que la plupart des QTL de résistance identifiés chez le blé tendre sont localisés sur les génomes A et B (Buerstmayr et al. 2009), le rôle du génome D, absent chez le blé dur, est susceptible de jouer un rôle déterminant dans la stimulation de la résistance à la fusariose [START_REF] Fakhfakh | Inheritances of Fusarium head blight resistance in a cross involving local and exotic durum wheat cultivars[END_REF].

Afin de pallier aux différences de ploïdie, des sources de résistance ont été criblées chez les autres espèces de blé tétraploïdes. Les espèces sauvages apparentées ont développé une large adaptation génétique aux stress biotiques et offrent un important réservoir de gènes pour l'amélioration du blé dur. Différentes études ont identifié des accessions modérément résistantes à la fusariose chez les blés tétraploïdes T. dicoccoides, T. dicoccum et T. carthlicum.

L'ancêtre du blé dur, T. dicoccoides, a été intensément étudié. Miller et al. (1998) ont criblé 290 accessions de T. dicoccoides issus de la collection de l'USDA pour leur réponse à la fusariose et ont identifié plusieurs accessions présentant des bons niveaux de résistance de type 2. (Buerstmayr et al. 2003b) ont évalué 151 lignées, originaires principalement d'Israël, et ont identifié huit accessions avec un bon niveau de résistance. De même, une large collection, comprenant 416 accessions de T. dicoccoides d'origines diverses, a été évaluée par Oliver et al. (2007). Une large variation pour la réponse à la fusariose a été signalée par les auteurs, avec plusieurs accessions possédant un haut niveau de résistance. Enfin, Oliver et al. (2008) ont criblé 376 accessions de différentes espèces de blé tétraploïde et ont identifié 16 T. carthlicum et quatre T. dicoccum avec des niveaux de résistance à la fusariose modérés à hautement résistant. Ces accessions de blé tétraploïde sont des sources de résistance intéressantes pour l'amélioration du blé dur. Elles ont été jusqu'à présent peu utilisées dans les programmes de sélection. Aucune de ces accessions n'est comparable à Sumai-3 en termes de niveaux de résistance. De plus, l'incorporation d'espèces sauvages apparentées dans les programmes de sélection de blé dur élite pose des difficultés du fait de leurs caractéristiques exotiques. Pour réduire le transfert d'allèles défavorables lors de l'introgression d'un allèle favorable (linkage drag), fréquemment rencontré lors de l'utilisation de matériel sauvage ou exotique, des techniques de substitution chromosomiques ont été utilisées pour transférer la résistance de T. dicoccoides vers le blé dur. Stack et al. (2002) ont ainsi évalué des lignées de substitution disomiques de l'accession, modérément résistante, de T. dicoccoides Israel-A dans le fond génétique du cultivar de blé dur Langdon. Les lignées de substitution portant le chromosome 3A de T. dicoccoides présentaient des meilleurs niveaux de résistance. De la même façon, les lignées de substitution portant le chromosome 7A de l'accession de T. dicoccoides PI478742, présentaient également une meilleure résistance à la fusariose.

Les progrès réalisés en ingénierie et manipulation chromosomique ont permis l'utilisation d'espèces plus éloignées, appartenant aux pools secondaires et tertiaire du blé dur. Certaines de ces espèces, du genre Leymus, Roegneria ou Thinopyrum, sont issues de régions dont le climat est favorable à la fusariose et certaines lignées possèdent une très haute, voire une complète, résistance à la maladie [START_REF] Cai | Utilization of alien genes to enhance Fusarium head blight resistance in wheat-a review[END_REF]. Elles représentent un précieux réservoir de gènes pour l'amélioration de la résistance à la fusariose. Un locus associé à la résistance a été identifié sur le chromosome 7E de T. elongatum et a été incorporé chez le blé tendre par l'utilisation de lignée de substitution et de translocation [START_REF] Fu | Molecular cytogenetic characterization of wheat-Thinopyrum elongatum addition, substitution and translocation lines with a novel source of resistance to wheat Fusarium head blight[END_REF]. Cette méthode est potentiellement utilisable également dans un fond génétique de blé dur. L'utilisation de ces espèces éloignées est toutefois entravée par leurs caractéristiques agronomiques défavorables. Une cartographie fine du locus à intégrer est en cours afin d'utiliser de manière efficace T. elongatum pour l'amélioration de la résistance à la fusariose [START_REF] Chen | The development of 7E chromosome-specific molecular markers for Thinopyrum elongatum based on SLAF-seq technology[END_REF]. La cartographie précise des locus de résistance de ces espèces éloignées permettra l'utilisation et l'incorporation des locus associés à la résistance dans des cultivars adaptés, tout en réduisant le transfert non désiré d'allèles défavorables.

Détection de QTL de résistance à la fusariose chez le blé tétraploïde

Jusqu'à présent, seules quelques sources de résistances tétraploïdes de T. dicoccoides, T. dicoccum, T. carthlicum et de landraces de T. durum ont été analysées par cartographie de QTL.

La plupart des études réalisées se sont intéressées à la résistance de type 2 après inoculation ponctuelle mesurée en serre et seulement deux études ont évalué la résistance globale de la sévérité à la maladie après inoculation en spray dans les champs. La majorité de ces analyses de QTL ont été faites sur des populations de taille limitée, susceptibles de réduire la capacité à détecter les QTL tout en surestimant leurs effets. Des QTL à effets faibles à modérés ont été principalement identifiés, localisés sur les chromosomes 2A, 2B, 3A, 3B, 4A, 4B, 5B, 6A, 6B, 7A et 7B. Plusieurs QTL ont été détectés dans des études indépendantes, tels que les QTL sur les chromosomes 2B, 3A, 3B et 6B, que l'on considère comme validées de manière indépendante. Le QTL sur 3A, à proximité du marqueur Xgwm2, a été signalé au sein de trois populations nonapparentées avec différentes accessions de T. dicoccoides comme source de résistance (Otto et al. 2002;[START_REF] Gladysz | Evaluation and genetic mapping of resistance to Fusarium head blight in Triticum dicoccoides[END_REF][START_REF] Chen | Saturation and comparative mapping of a major Fusarium head blight resistance QTL in tetraploid wheat[END_REF][START_REF] Buerstmayr | Genetic mapping of QTL for resistance to Fusarium head blight spread (type 2 resistance) in a Triticum dicoccoides × Triticum durum backcross-derived population[END_REF]. Ces trois accessions de T. dicoccoides portent probablement le même allèle de résistance à ce locus. Des variations alléliques peuvent être notées chez le blé tétraploïde au niveau du QTL détecté sur le chromosome 6B au sein de deux populations utilisant les accessions de T. dicoccum (Buerstmayr et al. 2012b) et T. carthlicum (Somers et al. 2006) comme sources de résistance. Ces deux différentes espèces tétraploïdes portent probablement des allèles différents au niveau du locus 6B.

La plupart des régions portant des QTL identifiés chez le blé tétraploïde correspondent à des QTL identifiés chez le blé tendre, suggérant une base génétique commune pour la résistance à la fusariose. Les QTL localisés sur les chromosomes 2A, 2B, 3A, 3B, 4A, 4B, 6B, 7A et 7B coïncident avec des QTL issus de différentes sources de résistances de blé tendre d'hiver et de printemps originaires d'Asie, d'Europe et d'Amérique du Nord [voir la revue publiée par Buerstmayr et al. (2009)]. Les QTL identifiés sur le chromosome 3B [START_REF] Ghavami | Mixed model association mapping for Fusarium head blight resistance in tunisianderived durum wheat populations[END_REF]Buerstmayr et al. 2012b) et 6B (Somers et al. 2006;Buerstmayr et al. 2012b), notamment, coïncident respectivement avec les QTL majeurs de résistance Fhb1 (Liu et al. 2008) et Fhb2 [START_REF] Cuthbert | Mapping of Fhb2 on chromosome 6BS: A gene controlling Fusarium head blight field resistance in bread wheat (Triticum aestivum L.)[END_REF]) issus tous deux de Sumai-3. Toutefois, la comparaison des allèles aux marqueurs associés à Fhb1 et Fhb2 effectuée par Buerstmayr et al. (2012b), a révélé différents haplotypes pour les lignées tétraploïdes et hexaploïdes. Ceci suggère une diversité génétique à ces loci et l'existence de différents allèles de résistance chez le blé dur et le blé tendre.

Les analyses de QTL réalisées chez le blé tétraploïde se sont principalement intéressées à des croisements du blé dur sensible avec une source de résistance apparentée. La plupart des allèles de résistance dérivent des blés tétraploïdes apparentés. Toutefois, les allèles de blé dur sont également associés à la résistance à la fusariose au niveau des QTL sur les chromosomes 2B (Somers et al. 2006;[START_REF] Gladysz | Evaluation and genetic mapping of resistance to Fusarium head blight in Triticum dicoccoides[END_REF]), 3B [START_REF] Ghavami | Mixed model association mapping for Fusarium head blight resistance in tunisianderived durum wheat populations[END_REF]Buerstmayr et al. 2012b) et 5B [START_REF] Ghavami | Mixed model association mapping for Fusarium head blight resistance in tunisianderived durum wheat populations[END_REF]). En dépit de sa sensibilité, le blé dur possède tout de même un certain niveau de résistance.

Des phénomènes de ségrégation transgressive pour la résistance à la fusariose ont été observés lors de croisement de lignées modérément sensibles ou modérément résistantes et, au sein de plusieurs populations, quelques lignées montrent moins de symptôme de fusariose que le parent résistant (Somers et al. 2006;[START_REF] Ghavami | Mixed model association mapping for Fusarium head blight resistance in tunisianderived durum wheat populations[END_REF]Ruan et al. 2012). Tirer parti de la ségrégation transgressive est prometteur pour le développement de lignées avec un meilleur niveau de résistance. Chez le blé tendre, Sumai-3 a été sélectionné à partir d'un croisement de deux parents modérément résistants. Son niveau exceptionnel de résistance peut s'expliquer par la combinaison d'allèles de résistance à différents loci, agissant principalement de manière additive [START_REF] Bai | Breeding for resistance to Fusarium head blight of wheat in China[END_REF]Schweiger et al. 2013).

L'existence d'interactions épistatiques et de facteurs de sensibilité qui modulent la résistance à la fusariose chez le blé tétraploïde a été signalée. Un QTL a été détecté sur le chromosome 2A de T. dicoccoides qui augmente la sensibilité à la fusariose quand il est transféré vers le blé dur. Ce locus pourrait agir comme un suppresseur de résistance et agir potentiellement de manière épistatique, réduisant l'effet d'autres QTL de résistance [START_REF] Garvin | Quantitative trait locus mapping of increased Fusarium head blight susceptibility associated with a wild emmer wheat chromosome[END_REF]. [START_REF] Ghavami | Mixed model association mapping for Fusarium head blight resistance in tunisianderived durum wheat populations[END_REF] ont également soupçonné l'existence de QTL qui module la réponse à la fusariose au niveau de la même région du chromosome 2A de blés durs tunisiens. L'existence d'interactions épistatiques a également été décrite par Somers et al. (2006) dans une population issue d'un croisement de blé dur avec T. carthlicum. Les QTL détectés sur les chromosomes 2A et 5A influencent l'effet du QTL de résistance sur le chromosome 6B. Il apparait ainsi important de contre-sélectionner ces facteurs génétiques qui augmentent la sensibilité ou qui diminuent la résistance à la fusariose.

Parmi les différentes analyses de QTL de résistance à la fusariose réalisées sur le blé tétraploïde, seules deux d'entre elles tiennent compte des caractères morphologiques et développementaux (Buerstmayr et al. 2012b;[START_REF] Buerstmayr | Genetic mapping of QTL for resistance to Fusarium head blight spread (type 2 resistance) in a Triticum dicoccoides × Triticum durum backcross-derived population[END_REF]. Il est généralement admis que ces caractères sont impliqués dans les mécanismes de résistance passifs. Bien que les caractères morphologiques aient un impact moins important sur le développement de la maladie après une inoculation ponctuelle, ils sont susceptibles d'avoir un effet important lors des évaluations en champs. Il est donc important de prendre ces effets en considération lors des études de résistance à la fusariose. Dans l'étude menée par Buerstmayr et al. (2012b), il apparait que ces caractères influencent la résistance à la fusariose du blé dur de la même façon que chez le blé tendre. Un QTL avec un fort effet sur la résistance a été détecté sur le chromosome 4B à la position du gène de nanisme Rht-B1 et un QTL détecté sur le chromosome 7B coïncide avec un QTL de précocité.

Chez le blé tendre, il est commun que des QTL de résistances coïncident avec les gènes Rht. Il n'est pas encore clairement établi si cette association est due à des effets pléiotropiques, à l'existence de gènes liés ou bien si elle est la conséquence de la hauteur des plantes per se. Les QTL de résistance associés à la hauteur des plantes peuvent avoir un impact négatif sur les performances agronomiques des lignées et sont donc inappropriés pour les programmes de sélection élites. La cartographie de QTL de caractères agronomiques importants doit ainsi être réalisée en concomitance avec la cartographie de QTL de résistance à la fusariose. Les QTL qui ne sont pas associés à des caractéristiques agronomiques indésirables sont à favoriser pour une amélioration efficace de la résistance à la fusariose dans les programmes de sélection.

Jusqu'à présent, seules les sources de résistance issues de blés tétraploïdes ont été exploitées pour l'amélioration de la résistance du blé dur. Les QTL de résistance détectés ne confèrent pas des niveaux de résistance équivalents à Fhb1, le QTL de résistance majeur identifié chez le cultivar de blé tendre Sumai-3 (Waldron et al. 1999;Anderson et al. 2001). Le blé dur n'a pas encore bénéficié des nombreux QTL détectés chez le blé tendre et les conséquences du transfert de Fhb1 du blé tendre vers le blé dur n'ont pas été communiquées à ce jour.

La deuxième partie de cette thèse rend compte de l'effet de Fhb1 au sein de trois populations biparentales développées par croisement de DBC-480 avec trois blés durs élites européens. DBC-480 est une lignée expérimentale de blé dur, résistante à la fusariose, qui possède l'allèle de résistance deFhb1 dérivé de Sumai-3. L'association de la résistance à la fusariose avec la hauteur des plantes est également décrite et, en particulier, l'effet de Rht-B1 et son interaction avec Fhb1 sur la sévérité de la maladie est examiné. Cette étude a fait l'objet d'une publication dans le journal Theoretical and Applied Genetics [START_REF] Prat | QTL mapping of Fusarium head blight resistance in three related durum wheat populations[END_REF].

Détection

Analyse statistiques des données phénotypiques

L'analyse des données a été réalisée sous R 3.1.3 (R development core team, 2016) en utilisant le paquet lme4 pour l'analyse des modèles mixtes (Bates et al. 2015)

Analyse QTL pour la taille des plantes et la date de floraison

Des QTL influant sur le caractère taille des plantes ont été détectés sur 4AL, 4BS, et 6AS. Dans les populations KD et DD, seulement un autre QTL majeur de résistance associé à la sévérité de la maladie a été détecté. Des effets similaires pour Fhb1 ont été observés. En revanche, pour la population SD, l'effet relatif de Fhb1 a été probablement diminué par la présence de trois autres QTL majeurs. L'effet de Fhb1 observé dans les populations de blé dur étudiées est analogue aux effets observés dans une série de lignées quasi-isogéniques de blé tendre par [START_REF] Pumphrey | Validating the Fhb1 QTL for fusarium head blight resistance in near-isogenic wheat lines developed from breeding populations[END_REF] où la sévérité de la maladie était réduite en moyenne de 23% et variant entre 0 et 70%. Lors de l'évaluation de la propagation de la maladie après inoculation ponctuelle, Fhb1 a présenté un large effet, expliquant 33% de la variation phénotypique. Ce résultat montre que, chez le blé dur,Fhb1 contribue principalement à la résistance de type 2. Cela est en accord avec ce qui a été précédemment établi chez le blé tendre où Fhb1 contribue principalement à la résistance de type 2 et, dans une moindre mesure, à la résistance de type 1 (Waldron et al. 1999;Anderson et al. 2001;[START_REF] Buerstmayr | Molecular mapping of QTLs for Fusarium head blight resistance in spring wheat. I. Resistance to fungal spread (type II resistance)[END_REF]Buerstmayr et al. 2003a;[START_REF] Cuthbert | Fine mapping Fhb1, a major gene controlling fusarium head blight resistance in bread wheat (Triticum aestivum L.)[END_REF]. Cette étude valide pour la première fois l'effet de Fhb1 dans un fond génétique de blé dur et marque une avancée significative pour l'amélioration de la résistance à la fusariose. Le blé tendre représente une ressource importante et utile pour l'amélioration du blé dur face à cette maladie car la plupart de ses QTL de résistance sont localisés sur les génomes A et B, communs au blé dur (Buerstmayr et al. 2009;Liu et al. 2009;Löffler et al. 2009).

Un QTL majeur de résistance sur 4BS, associé à la sévérité de la maladie, a été détecté au sein des trois populations étudiées. La localisation de ce QTL coïncide avec le gène Rht-B1. L'allèle de nanisme Rht-B1b est associé, dans les trois populations, à une plus grande sévérité de la maladie. Cette association a déjà été rapportée précédemment chez le blé tendre [START_REF] Hilton | Relationship between cultivar height and severity of Fusarium ear blight in wheat[END_REF][START_REF] Srinivasachary | Semidwarfing Rht-B1 and Rht-D1 loci of wheat differ significantly in their influence on resistance to Fusarium head blight[END_REF]. Des résultats équivalents ont également été trouvés dans trois populations de blé dur issues du rétrocroisement de l'accession résistante T. dicoccum-161 avec les cultivars semi-nains de blé durs Helidur, Floradur et DS-131621. Le QTL de résistance localisé au niveau du locus de Rht-B1 expliquait la plus grande partie de la variation phénotypique pour la sévérité de la maladie mesurée après inoculation en spray. De plus, dans ces trois populations, les individus possédant l'allèle Rht-B1b présentaient, aussi, un niveau plus élevé de symptômes (Buerstmayr et al. 2012b).

Au sein de la population SD, deux autres QTL majeurs ont été identifiés sur 4AL et 6AS. Ces deux QTL de résistance coïncident avec des QTL associés à la date de floraison et à la taille. Des QTL de résistance ont précédemment été détectés sur les chromosomes 4A et 6A chez le blé tétraploïde. Ils ont cependant été cartographiés sur des bras chromosomiques différents et leur localisation ne correspond pas à celle des QTL détectés dans cette étude. Plusieurs QTL de blé tendre ont, en revanche, été cartographiés dans la même région de 4AL chez les cultivars de blé tendre d'hiver Heyne [START_REF] Zhang | Quantitative trait loci for Fusarium head blight resistance in U.S. hard winter wheat cultivar Heyne[END_REF] et Arina [START_REF] Paillard | QTL analysis of resistance to Fusarium head blight in Swiss winter wheat (Triticum aestivum L.)[END_REF][START_REF] Buerstmayr | Comparative mapping of quantitative trait loci for Fusarium head blight resistance and anther retention in the winter wheat population Capo × Arina[END_REF]. Le QTL sur 6AS est localisé dans la même région que le QTL associé à la résistance de type 2 chez la lignée résistante de blé tendre ND2603 (Sumai 3/Wheaton) (Anderson et al. 2001).

Un QTL à effet mineur a été cartographié dans la population KD sur 2BL à proximité du centromère. Des QTL de résistance ont été identifiés dans cette région dans deux populations de blé tétraploïde. Pour ces QTL, l'allèle de résistance dérive des parents de blé dur sensibles à la fusariose, Strongfield (Somers et al. 2006) et Helidur [START_REF] Gladysz | Evaluation and genetic mapping of resistance to Fusarium head blight in Triticum dicoccoides[END_REF].

Dans la population DD, un QTL a été identifié sur 5AL. Un effet majeur de ce QTL a été détecté en 2013 alors qu'il n'a eu aucun effet en 2014 et 2015. Il semble que ce QTL n'est pas localisé dans la même région que le QTL majeur de résistance du blé tendre Qfhs.ifa-5A issu de Sumai-3 (Buerstmayr et al. 2003a).

  Mots clés : blé dur, Triticum durum, fusariose de l'épi, QTL, résistance, Fhb1 Zusammenfassung Ährenfusariose (FHB) wird durch die Pilze Fusarium culmorum und Fusarium graminearum verursacht und ist eine Pflanzenkrankheit, welche weltweit verheerende Ausmaße im Getreideanbau annehmen kann. Der Befall mit FHB hat erhebliche Ernteverluste sowie starke Qualitätseinbußen des Ernteguts zur Folge und verursacht somit massive wirtschaftliche Schäden. Durch die Anreicherung von Mykotoxinen, z.B. Deoxynivalenol (DON), im Erntegut befallener Pflanzen stellt FHB aber auch eine direkte Gefahr für Tier und Mensch dar. Kontaminierte Lebens-und Futtermittel sind für den Gebrauch nicht mehr geeignet, da mit ernsthaft negativen Auswirkungen auf die Gesundheit zu rechnen ist. Eine Schlüsselrolle im erfolgreichen Krankheitsmanagement von FHB spielt die Wirtsresistenz: Diese wird als die kostengünstigste und nachhaltigste Methode angesehen den Befall mit FHB und folglich auch die Mykotoxinverunreinigung zu minimiren. FHB Resistenz ist ein quantitativ vererbtes Merkmal und wird von sogenannten "quantitative trait loci" (QTL) gesteuert, welche gemeinsam die Resistenz bewerkstelligen. Die extreme Anfälligkeit von Durumweizen (Triticum durum Desf.) stellt in Kombination mit der fehlenden genetischen Variabilität betreffend FHB Resistenz im primären Genpool für die Züchtung resistenter Sorten eine große Herausforderung dar. Im ersten Teil der vorliegenden Arbeit wurde zunächst eine Zusammenstellung von aktuell vorhandenem Wissen über die Genetik von FHB Resistenz in Durumweizen erarbeitet. Die genetischen Ressourcen, welche für die FHB Resistenzzüchtung bei Durumweizen zur Verfügung stehen wurden erhoben und umfassen sowohl eng verwandte als auch fremde Arten. Bis dato publizierte Ergebnisse von QTL Kartierungen in tetraploidem Weizen wurden zusammengefasst und miteinander verglichen: in Summe konnten 13 Resistenz QTL identifiziert werden, welche in unterschiedlichen Umwelten und unabhängigen Studien wiederholt aufgefunden wurden. Derartige QTL können als stabil angesehen werden und eignen sich daher besonders für Verwendung in Züchtungsprogrammen. Des Weiteren zeigte sich, dass die meisten Resistenz QTL in tetraploidem Weizen mit denen in hexaploidem Weizen (Triticum aestivum L.) überlappenwas auf eine gemeinsame genetische Basis der FHB Resistenz hindeutet.

Introduction

Figure 1 :

 1 Figure 1: Phylogeny of wheat species

[

  teleomorph: Gibberella avenacea], Fusarium poae [teleomorph unknown], Microdochium nivale [teleomorph: Monographella nivalis var. nivalis]. and Microdochium majus

Figure 2 :

 2 Figure 2: The life cycle of Fusarium. graminearum [teleomorph: Gibberella zeae] causing Fusarium head blight on wheat under field condition (modified from Trail 2009)

Figure 3 :

 3 Figure 3: Durum wheat heads showing Fusarium head blight symptoms with premature bleached spikelets

  variance explained by the QTL b Numbers in square brackets for cross reference with Fig. 1 c FHB index: calculated by multiplying the disease incidence by the disease severity d Not estimated

  ) quantitative trait locus (QTL) Fhb1 was assessed for the first time in durum wheat. Three F7-RIL mapping populations of about 100 lines were developed from crosses between the durum wheat experimental line DBC-480, which carries an Fhb1 introgression from Sumai-3, and the European T. durum cultivars Karur, Durobonus and SZD1029K. The RILs were evaluated in field experiments for FHB resistance in three seasons using spray inoculation and genotyped with SSR as well as genotyping-by-sequencing markers. QTL associated with FHB resistance were identified on chromosome arms 2BL, 3BS, 4AL, 4BS, 5AL and 6AS at which the resistant parent DBC-480 contributed the positive alleles. The QTL on 3BS was detected in all three populations centered at the Fhb1 interval. The Rht-B1 locus governing plant height was found to have a strong effect in modulating FHB severity in all populations. The negative effect of the semi-dwarf allele Rht-B1b on FHB resistance was compensated by combining with Fhb1 and additional resistance QTL. The successful deployment of Fhb1 in T. durum was further substantiated by assessing type 2 resistance in one population. The efficient introgression of Fhb1 represents a significant step forward for enhancing FHB resistance in durum wheat.

  among which resistance to initial infection (type 1) and resistance to fungal spread within infected spikes (type 2) are commonly accepted and have been widely investigated in QTL mapping studies. Under field conditions, overall FHB resistance is usually assessed through scoring of disease severity after spray inoculation and is considered to reflect the genotypic response during natural epidemics. Both active and passive mechanisms influence FHB resistance (Mesterházy 1995). The latter include morphological and developmental features which affect primary fungal infection and/or disease development through disease escape mechanisms. Plant height is one of the foremost morphological traits affecting FHB response and the widely deployed Norin 10 semi-dwarfing Rht alleles, namely

  mapping populations comprising 111, 100 and 100 F 7 RILs were developed by single seed descent from crosses of the tetraploid resistant line DBC-480 to the susceptible European T. durum cultivars Karur (KD) and Durobonus (DD) and the advanced breeding line SZD1029K (SD), respectively. Karur and Durobonus are registered varieties bred by RAGT, France (registered 2002) and Saatzucht-Donau, Austria (registered 2004), respectively. The breeding line SZD1029K was provided by Saatzucht-Donau for this study. Experimental line DBC-480 was developed at IFA-Tulln, Austria by four generations of marker-assisted backcrossing of the highly resistant T. aestivum cultivar Sumai-3 into the background of the Austrian T. durum variety Semperdur and subjected to rigorous phenotypic selection for improved FHB resistance in field trials (details not shown). The presence of the resistant allele at Fhb1 was verified using the SSR markers Xgwm389, Xgwm533 and Xgwm493. Karur, Durobonus and SZD1029K possess the semi-dwarfing allele Rht-B1b, while DBC-480 is a tall line that harbours the Rht-B1a wild type allele.FHB resistance phenotypingThe three mapping populations along with their parental lines were evaluated in multiple field experiments at IFA-Tulln, Austria (16°04,16′E, 48°19,08′N, 177 m above sea level) in 2013, 2014 and 2015. Experiments were laid out as randomized complete block designs with two blocks in 2013 and three blocks in 2014 and 2015. Plots consisted of single rows in 2013 and double rows of 1 m length at 17 cm spacing in 2014 and 2015. Sowing of the individual blocks was performed in early spring and staggered one to two weeks apart leading to slightly different flowering dates between the blocks. Management of the field trials was conducted

Fig. 1 FHB

 1 Fig. 1 Scatterplots and marginal histogram of frequency distribution of overall means for FHB severity (AUDPC) against plant height (cm) measured in the field trials for each population (A, B, C) and for FHB spread (PIS) against plant height (cm) measured in the greenhouse trials for KD population (D). Parents are indicated by arrows

Fig. 3

 3 Fig. 3 Boxplot distributions of RILs according to their allele combinations at the FHB resistance loci for the KD (A) and DD (B) populations for overall mean FHB severity (AUDPC). Medians are indicated by solid lines, points represent outliers. For each subgroup, the number of lines, mean values and standard deviations of FHB severity (AUDPC) and plant height (cm) are indicated. Values followed by different letters are significantly different (p < 0.05) based on Tukey test

  Molecular mapping of QTLs for Fusarium head blight resistance in spring wheat. I. Resistance to fungal spread (type II resistance). Theor Appl Genet 104:84-91 Buerstmayr H, Steiner B, Hartl L, Griesser M, Angerer N, Lengauer D, Miedaner T, Schneider B, Lemmens M (2003a) Molecular mapping of QTLs for Fusarium head blight resistance in spring wheat. II. Resistance to fungal penetration and spread. Theor Appl Genet 107:503-508 Buerstmayr H, Steiner B, Lemmens M, Ruckenbauer P (2000) Resistance to Fusarium head blight in winter wheat: heritability and trait associations. Crop Sci 40:1012-1018 Buerstmayr H, Stierschneider M, Steiner B, Lemmens M, Grisser M, Nevo E, Fahima T (2003b) Variation for resistance to head blight caused by Fusarium graminearum in wild emmer (Triticum dicoccoides) originating from Israel. Euphytica 130:17alleles Rht-D1b and Rht-B1b show marked differences in their associations with anther-retention in wheat heads and with Fusarium head blight susceptibility. Phytopathology. doi:10.1094/PHYTO-05-16-0200-R Buerstmayr M, Huber K, Heckmann J, Steiner B, Nelson J, Buerstmayr H (2012) Mapping of QTL for Fusarium head blight resistance and morphological and developmental traits in three backcross populations derived from Triticum dicoccum × Triticum durum. Wei Y, Cao W, Lan X, Yu M (2010) Confirmation of the relationship between plant height and Fusarium head blight resistance in wheat (Triticum aestivum L.) by QTL meta-analysis. Euphytica 174:343Validating the Fhb1 QTL for fusarium head blight resistance in nearisogenic wheat lines developed from breeding populations Crop Sci 47:200-206 R Core Team (2015) R: A language and environment for statistical computing. http://www.R-project.org/. Effects of introgression of two QTL for fusarium head blight resistance from Asian spring wheat by marker-assisted backcrossing into European winter wheat on fusarium head blight resistance, yield and quality traits. Mol Breed 28:485candidate genes in the divergent haplotype encoding Fhb1, a major Fusarium head blight resistance locus in wheat. Theor Appl Genet 129:1607-1623. Somers D, Fedak G, Clarke J, Cao W (2006) Mapping of FHB resistance QTLs in tetraploid wheat. Genome 49:1586-1593 Somers DJ, Isaac P, Edwards K (2004) A highdensity microsatellite consensus map for bread wheat (Triticum aestivum L.). Theor Appl Genet 109:1105-1114 Song QJ, Shi JR, Singh S, Fickus EW, Costa JM, Lewis J, Gill BS, Ward R, Cregan PB (2005) Development and mapping of microsatellite (SSR) markers in wheat. Theor Appl Genet 110:550-560 Srinivasachary, Gosman N, Steed A, Hollins T, Bayles R, Jennings P, Nicholson P (2009) Semi-dwarfing Rht-B1 and Rht-D1 loci of wheat differ significantly in their influence on resistance to Fusarium head blight. Bai G, Bockus W, Ji X, Pan H (2012) Quantitative trait loci for Fusarium head blight resistance in U.S. hard winter wheat cultivar Heyne. Crop Sci 52:1187-1194 Zhu X, Zhong S, Cai X (2016a) Effects of Dgenome chromosomes and their A/Bgenome homoeologs on Fusarium head blight resistance in durum wheat. Crop Sci 56:1-10 Zhu X, Zhong S, Chao S, Gu YQ, Kianian SF, Elias E, Cai X (2016b) Toward a better understanding of the genomic region harboring Fusarium head blight resistance QTL Qfhs.ndsu-3AS in durum wheat. Theor Appl Genet 129:31-43 Conclusion Fusarium head blight is considered one of the most important disease affecting durum wheat and common wheat production because of its damaging effect on grain production, including yield and quality losses, its deleterious effect on food safety and the intensifying disease pressure reported in cropping regions in the last few decades. The cultivation of resistant cultivars is pivotal to efficiently control FHB and breeding for increased resistance has consequently become an important objective. Common wheat has benefited from great research efforts and improved cultivars have been identified. In comparison, durum wheat, considered a minor crop on a global scale, has received little attention and the need to develop cultivars with enhanced resistance is pressing. The identification and understanding of genetic factors underlying FHB resistance in durum wheat is a prerequisite for successful resistance breeding. The review paper, set up in the course of this work, represents the first summary focusing specifically on the results from QTL mapping investigations performed in tetraploid wheat. This paper provides the durum wheat breeding and research community an extensive overview for future investigations.

  Comparison of Somers et al. (2004) and Marone et al. (2012) consensus map near the approximate QTL positions which are indicated by vertical bars. For readability only selected markers are shown. The complete maps with all mapped

  (a) Linkage map based on Somers et al. (2004) (b) Linkage map based on Marone et al. (2012) (c) Linkage map based on Ghavami et al. (2011) , genotype × year σ 2 Genotype×Year and the residual effects σ 2 error for FHB severity (AUDPC), plant height (cm) and flowering date (days after May 1st) across three experiments for the KD, DD and SD populations Online Resource 1_B: Variance component estimates of genotype σ 2 Genotype , Experiment σ 2 Exp , and the residual effects σ 2 error for FHB spread (percent infected spikelets PIS) and plant height (cm) in the KD population across three unreplicated experiments Online Resource 2: Pearson correlation coefficients between FHB severity, FHB spread, plant height and flowering date in individual experiments for the KD, DD and SD populations Online Resource 3: Marker distribution in the KD, DD and SD populations Online Resource 4: Chromosome locations and positions of markers in linkage map of the KD, DD and SD populations

  risque sanitaire. Ce problème est d'autant plus inquiétant dans la production du blé dur qu'elle est essentiellement utilisée pour l'alimentation humaine. Le déoxynivalénol (DON) et ses dérivés, sont les mycotoxines les plus fréquemment rencontrées lors d'infections par Fusarium. Le DON perturbe le fonctionnement des cellules eucaryotes et induit notamment une inhibition de la synthèse protéique (Pestka 2010). Des recommandations ou régulations ont ainsi été mises en place par plusieurs Etats afin de limiter la teneur totale en DON des produits céréaliers bruts destinés à l'alimentation humaine et animale. La Commission Européenne, par exemple, a mis en place une règlementation stricte de la teneur maximale en DON avec un seuil de 1.25 ppm pour le blé tendre et de 1.75 ppm pour le blé dur (Official Journal of the European Communities 2007). La règlementation s'applique aussi aux produits transformés tels que les pâtes (0.7 ppm), le pain et produits de boulangerie (0.5 ppm) et les aliments pour nourrissons (0.2 ppm). De même, l'Agence américaine des produits alimentaires et médicamenteux (Food and Drug Administration, FDA) des Etats-Unis a introduit depuis 1993 une recommandation du seuil maximal de DON à 1 ppm pour les produits céréaliers destinés à l'alimentation humaine (Guidance for Industry and FDA 2010). Les lots dont la teneur en DON excède les limites acceptables sont susceptibles d'être dévalués ou refusés contribuant ainsi à des pertes économiques supplémentaires pour les producteurs de blés. Ces dernières décennies, plusieurs facteurs ont accentué le risque d'épidémie de fusariose.

  de QTL de résistance à la fusariose au sein de trois populations apparentées de blé dur MATERIELS ET METHODES Matériel végétal Le matériel végétal utilisé dans cette étude consiste en trois populations biparentales contenant 111, 100 et 100 F 7 RIL (lignées pures recombinantes ou « recombinant inbred lines) issues, respectivement, de croisement de la lignée expérimentale de blé dur, résistante à la fusariose, DBC-480, avec les cultivars sensibles de blé dur Karur (KD), Durobonus (DD) et SZD1029K (SD). Karur et Durobonus sont des variétés inscrites au catalogue et sélectionnées respectivement par RAGT (inscription en 2002) et Saatzucht-Donau (inscription en 2004). SZD1029K est une lignée issue des programmes de sélection de Saatzuch-Donau. La lignée expérimentale tétraploïde DBC-480 a été développée à l'IFA-Tulln en Autriche par quatre générations de rétrocroisement assisté par marqueurs de la variété de blé tendre Sumai-3 avec la variété de blé dur autrichienne Semperdur puis soumise à une sélection phénotypique rigoureuse en champ pour sa résistance à la fusariose. L'introgression de Fhb1 a été vérifiée en utilisant les marqueurs SSR Xgwm389, Xgwm533 et Xgwm493. Karur, Durobonus et SZD1029K possèdent l'allèle de nanisme Rht-B1b ; au contraire de DBC-480 qui est une lignée haute, possède l'allèle sauvage Rht-B1a. Phénotypage de la résistance à la fusariose Les trois populations biparentales, ainsi que les lignées parentales, ont été évaluées au sein de plusieurs essais en champs en 2013, 2014 et 2015, à l'IFA-Tulln en Autriche. Les essais ont été disposés en blocs complets randomisés avec deux blocs en 2013 et trois blocs en 2014 et 2015. Les essais ont été inoculés en spray, lors de la floraison, par une suspension d'un isolat de Fusarium culmorum Fc91015, à une concentration de 2.5 x 10 4 ml -1 . Afin de faciliter la germination des spores et le développement de la maladie, la canopée a été maintenue humide par brumisation durant 20h après chaque cycle d'inoculation. La sévérité de la maladie a été estimée visuellement comme le pourcentage d'épillets infectés au sein de chaque plot à 14, 18, 22 et 26 jours après la date de floraison. En 2013, la notation a été réalisée à 18 et 26 jours après la floraison. L'aire sous la courbe de développement de la maladie (AUDPC ou « area under disease progress curve ») a été calculée et utilisée comme mesure intégrée de la résistance à la sévérité de la maladie. La taille des plantes a également été mesurée en centimètre et la date de floraison notée et convertie en nombre de jours après le 1 er mai. La population KD et les parents Karur et DBC-480 ont également été testés en serre pour la résistance à la propagation dans l'épi, ou résistance de type 2, après inoculation ponctuelle au sein de trois essais non-répliqués à Florimond-Desprez, France, au cours de l'hiver 2015 (GH1) et à l'IFA-Tulln, Autriche, en été 2016 (GH2 et GH3). L'inoculation ponctuelle a été réalisée à la floraison en pipetant 10 µl d'inoculum de F. culmorum Fc91015, à la même concentration que pour les essais inoculés en spray, entre les glumelles et les paléas de quatre épillets situés au centre de l'épi. Pour favoriser l'infection par le pathogène, les épis ont été couverts par des sacs transparents de polyéthylène durant 24h après l'inoculation. La résistance de type 2 a été mesurée par le pourcentage d'épillets infectés (PIS) 24 jours après inoculation en comptant le nombre d'épillets infectés et le nombre total d'épillets pour chaque épi. En moyenne, huit épis par génotype ont été inoculés pour chacun des essais. Pour chaque lignée, la hauteur des plantes a également été mesurée.

  L´allèle permettant l´augmentation de la taille provient à chaque fois du parent DBC-480. Le locus Rht-B1b a été identifié au sein des trois populations et explique respectivement 95%, 81% et 37% de la variation pour PH dans les populations KD, DD et SD. Dans la population SD, deux autres QTL sont associés à la hauteur des plantes sur 4AL et 6AS expliquant 11% et 27% de la variation. Ces QTL exercent un effet épistatique sur le locus Rht-B1 bien que considéré comme faible comparé à leurs effets additifs. L'analyse de QTL pour la date de floraison a permis la détection de QTL sur les chromosomes 1BL, 2BS, 4AL, 5AL, 6AS et 6BS. L'allèle de DBC-480 confère une précocité plus tardive pour les QTL sur 2BS, 4AL, 5AL, 6AS et 6BS. Le QTL sur 2BS a été identifié sur la même région dans les trois populations et est localisé dans une région distale du QTL associé à la sévérité de la maladie identifié sur 2BL dans la population KD. Dans la population SD, les QTL associés à la sévérité de la maladie, la hauteur des plantes et la date de floraison, coïncident sur 4AL et 6AS. Ces loci semblent posséder des effets pléiotropiques.Co-localisation entre les QTL de taille et ceux de résistanceL´idéotype recherché par le sélectionneur de blé dur est une variété semi-naine avec une résistance améliorée à la fusariose. Pour vérifier la faisabilité d'un tel idéotype au sein des populations étudiées, les effets des QTL de résistance détectés ont été comparés. Dans la population SD, trois QTL majeurs de résistance ont coïncidé avec des QTL associés à la hauteur des plantes. L'effet de Fhb1, le seul QTL qui ne soit pas associé à la hauteur dans cette population, n'a pas contrebalancé l'effet négatif des allèles de nanismes aux loci Rht-B1, 4AL et 6AS, qui confèrent une plus grande sensibilité à la fusariose. Dans les populations KD et DD, trois QTL, dont Fhb1, sont associés à la résistance à la maladie et, parmi eux, seul le locus Rht-B1 est associé à la fois à la résistance et à la hauteur des plantes. Les individus possédant l'allèle de nanisme Rht-B1b ont été significativement plus petits et plus sensibles que les individus possédant l'allèle sauvage Rht-B1a. La hauteur des plantes, pour les individus portant l'allèle Rht-B1b, était réduite de 31% et 25% en moyenne pour les populations KD et DD respectivement, et les niveaux de sévérité de la maladie étaient multipliés par deux en comparaison aux individus portant l'allèle Rht-B1a. Toutefois, dans la population KD, les individus portant les allèles de résistance sur Fhb1 et 2BL en combinaison avec Rht-B1b ont présenté des niveaux de sévérité réduits de 38% comparé aux lignées naines ne portant aucun QTL de résistance tout en montrant un niveau de résistance équivalent aux lignées portant l'allèle Rht-B1a et aucun QTL de résistance. Dans la population DD, les individus portant les allèles de résistance sur Fhb1 et 5AL en combinaison avec Rht-B1b ont vu les niveaux de sévérité réduits de 53% par rapport aux lignées naines sans QTL de résistance. De même, leur niveau de résistance n'a statistiquement pas été différent de celui des lignées portant l'allèle Rht-B1a. Ces résultats montrent que, dans ces populations, la combinaison des allèles de résistance aux différents QTL compense efficacement l'effet négatif de Rht-B1b sur la résistance à la fusariose.DISCUSSIONL'amélioration de la résistance du blé dur à la fusariose est devenue ces dernières années une priorité dans les programmes de sélection. Le nombre limité de sources de résistance disponible chez le blé dur a poussé les sélectionneurs à exploiter la résistance dérivée d'espèces apparentées.Dans cette étude, le blé tendre a été utilisé pour la première fois comme source de résistance dans un fond génétique de blé dur. La lignée tétraploïde résistante DBC-480, qui porte le QTL majeur de résistance Fhb1, présentait un bon niveau de résistance après inoculation artificielle dans les champs et en serre. L'utilisation de trois différentes populations biparentales a permis de disséquer les bases génétiques de la résistance à la fusariose tout en validant les effets des QTL détectés au sein de différents fonds génétiques de blé dur élite.Architecture génétique de la résistance à la fusarioseL'architecture génétique de la résistance à la fusariose dans les trois populations est quantitative et de nature oligo-à polygénique. Au total six QTL associés à la résistance à la fusariose ont été détectés sur les bras chromosomiques 2BL, 3BS, 4AL, 4BS, 5AL et 6AS. L'allèle de résistance dérive de DBC-480 à tous ces loci. La comparaison de la position des QTL identifiés avec la carte consensus fournie par DArT PL (A.Kilian, Diversity Arrays Technologies, communication personelle, 2016) et les cartes génétiques publiées parSomers et al. (2004) etMarone et al. (2012), montre que les QTL détectés dans cette étude coïncident avec des régions où des QTL ont préalablement étaient identifiés chez le blé tendre et le blé dur.Le QTL détecté sur 3BS, à proximité des marqueurs Xbarc147 et Xumn10, correspond au locus de Fhb1. Des variations de l'effet de Fhb1 sur la sévérité de la maladie ont été observées et expliquent entre 5% et 16% de la variance phénotypique en fonction du fond génétique de blé dur et de l'essai considéré. L'allèle de résistance à Fhb1 est associé à une réduction des symptômes de sévérité de la maladie de 30% en moyenne dans la population KD et de 36% dans la population DD alors que dans la population SD cette réduction est de 6% seulement. Cette disparité, observée entre les populations KD et DD d'un côté et la population SD de l'autre, peuvent être attribuées à leurs différentes architectures génétiques pour la résistance à la maladie.

  Association des QTL pour la résistance à la fusariose, la date de floraison et la hauteur des plantes Dans cette étude, parmi les six QTL associés à la date de floraison, deux d'entre eux coïncident avec des QTL de résistance sur 4AL et 6AS dans la population SD. Ces deux QTL ont un effet fort sur ces deux caractères et une corrélation positive a été observée entre la date de floraison et la sévérité de la maladie dans cette population. Dans les populations KD et DD, une corrélation faible ou non significative a été trouvée entre les deux caractères et lorsque les essais sont analysés séparément, les corrélations varient considérablement. Ces résultats ne laissent apparaitre aucune tendance générale quant à l'association de ces caractères. Cela peut-être expliqué par l'absence de QTL coïncidant pour ces caractères dans les populations KD et DD. La variabilité des corrélations observées reflète certainement la variation des conditions environnementales locales au moment de la floraison et de l'inoculation, influençant le développement de la maladie.Au contraire, la hauteur des plantes est négativement et significativement corrélée à la sévérité de la maladie au sein des trois populations. Cela est en accord avec les résultats observés précédemment dans d'autres populations de blé dur(Talas et al. 2011; Buerstmayr et al. 2012b; Miedaner and Longin 2014). Tous les QTL de hauteur des plantes identifiés dans cette étude coïncident avec des QTL associés à la sévérité de la maladie sur les QTL 4AL, 4BS et 6AS. La coïncidence de QTL de hauteur de la plante et de sévérité est couramment observée chez le blé et est appuyée par les résultats de méta-analyse de QTL[START_REF] Mao | Confirmation of the relationship between plant height and Fusarium head blight resistance in wheat (Triticum aestivum L.) by QTL metaanalysis[END_REF]. Les mécanismes sousjacents à l'association de ces deux caractères sont complexes et peuvent être attribués aux effets de différence de hauteur des plantes per se et/ou à des effets pléiotropiques des gènes de nanismes ou à l'existence de gènes liés qui augmentent la sensibilité à la fusariose. Dans cette étude, en raison de la grande variation de hauteur des plantes observées, avec des différences d'environ 60 cm entre les plantes les plus petites et les plus hautes, une partie de cette association peut être attribuée à la hauteur des plantes per se. En dépit d'une inoculation en spray des épis et en assurant une brumisation homogène, les épis des plantes semi-naines ont tendance à rester plus humides et donc sous des conditions de pression d'infection plus fortes, que les épis des plantes hautes. Cela est en accord avec les conclusions tirées parBuerstmayr et al. (2012b) lors de l'évaluation de la sévérité de la fusariose de trois populations de blé tétraploïdes présentant des variations pour la hauteur des plantes similaires à celles observées dans cette étude. Les auteurs supposent un évitement de l'infection pour les plantes les plus hautes, et ce, malgré la mise en place d'un système de brumisation contrôlé après inoculation en spray.Perspectives pour l'amélioration du blé dur pour la résistance à la fusariose et conclusionIl apparait clairement que, dans ces populations, la hauteur des plantes exerce une forte influence en modulant la réponse à la fusariose. La plus grande sensibilité à la fusariose observée chez les plantes semi-naines, et associée à Rht-B1b, est un défi pour les sélectionneurs. Rht-B1b confère des caractéristiques agronomiques bénéfiques, liées à un rendement et un indice de récolte plus important, tout en permettant l'obtention de plantes semi-naines qui réduisent le risque de verse dans les systèmes de production agricoles modernes practices(Royo et al. 2007; Subira et al. 2016). Cette étude montre que la présence de Fhb1, associé à un QTL mineur de résistance, permet la sélection de lignées semi-naines possédant un meilleur niveau de résistance à la fusariose. Ces résultats sont en accord avec les résultats obtenus chez le blé tendre où la combinaison de deux QTL contrebalance l'effet négatif de l'allèle de nanisme Rht-D1b et permet l'amélioration de la résistance des lignées semi-naines[START_REF] Lu | Two major resistance quantitative trait loci are required to counteract the increased susceptibility to fusarium head blight of the Rht-D1B dwarfing gene in wheat[END_REF]. Les lignées des populations KD et DD possédant la combinaison d'allèles favorables aux loci Rht-B1 et Fhb1, ainsi que l'allèle de résistance sur 2BL ou 5AL, représentent une ressource nouvelle et unique pour l'amélioration de la résistance du blé dur à la fusariose. Le matériel végétal développé dans cette étude est proche agronomiquement du germoplasme moderne européen. Les lignées améliorées sélectionnées sont ainsi facilement incorporables dans les programmes de sélection de blé dur en vue d'améliorer la résistance à la fusariose.

Figure 3

 3 Figure 3 Boxplot distributions of RILs according to their allele combinations at the FHB resistance loci for the KD (A) and DD (B) populations for overall mean FHB severity (AUDPC). Medians are indicated by solid lines, points represent outliers. For each subgroup, the number of lines, mean values and standard deviations of FHB severity (AUDPC) and plant height (cm) are indicated. Values followed by different letters are significantly different (p < 0.05) based on Tukey test………………...…………………..52

Table 1

 1 Information on mapping populations and the phenotyping methods performed for mapping Fusarium resistance QTL in tetraploid wheat

	Plant material		Phenotyping			References
	Parents	Population	Number of exp. a	IM b	Iso c
	Langdon(Dic-3A) 9 Langdon	83 RIL	2 GH	SFI	Fg	Otto et al. (2002)
	Langdon(Dic-3A) 9 Langdon	83 RIL	2 GH	SFI	Fg	Chen et al. (2007)
	Langdon(Dic-7A) 9 Langdon	118 RIL	3 GH	SFI	Fg	Kumar et al. (2007)
	Langdon(Dic-2A) 9 Langdon	63 RIL	3 GH	SFI	Fg	Garvin et al. (2009)
	Strongfield 9 Blackbird	85 DH	1 GH	SFI	Fg	Somers et al. (2006)
	Mt. Hermon#22 9 Helidur	140 BC 1 F 5	1 GH, 2 Field	SFI	Fc	Gladysz et al. (2007)
	Tun34 9 Lebsock	169 BC 1 F 6	2 GH	SFI	Fg	Ghavami et al. (2011)
	Multi-parental association	171 BC 1 F 7 and 169 BC 1 F 6	2 GH	SFI	Fg	Ghavami et al. (2011)
	mapping population
	Td161 9 Floradur	129 BC 1 F 4	4 Field	SPI	Fg, Fc	Buerstmayr et al. (2012b)
	Td161 9 DS-131621	134 BC 1 F 4	4 Field	SPI	Fg, Fc	Buerstmayr et al. (2012b)
	Td161 9 Helidur	126 BC 1 F 4	4 Field	SPI	Fg, Fc	Buerstmayr et al. (2012b)
	BGRC3487/2 9 DT735	160 BC 1 RIL	4 Field	SPI	Fg, Fc	Ruan et al. (2012)
	Mt. Gerizim#36 9 Helidur	103 BC 1 F 6	4 GH	SFI	Fc	Buerstmayr et al. (2013)

a Number of experiments: GH greenhouse experiment, Field field experiment b Inoculation method: SFI single-floret inoculation, SPI spray inoculation c Isolate used for inoculation: Fg F. graminearum, Fc F. culmorum Table 2

List of QTL in tetraploid wheat. Information on location and associated markers, magnitude of QTL effect on the Fusarium-related trait evaluated, parent contributing to the resistant allele as well as association with other traits and co-localization with major hexaploid wheat QTL are included

  DNA markers for Fusarium head blight resistance QTLs in two wheat populations. Theor Appl Genet 102:1164-1168 Atanasoff D (1920) Fusarium-blight (scab) of wheat and other cereals. J Agric Res 20:1-32 Bai GH, Shaner G (2004) Management and resistance in wheat and barley to Fusarium head blight. Annu Rev Phytopathol 42:135-161 Bai GH, Desjardins AE, Plattner RD (2001) Deoxynivalenol non producing Fusarium graminearum causes initial infection, but does not cause disease spread in wheat spikes. Mycopathologia 153:91-98 Bai GH, Chen LF, Shaner G (2003) Breeding for resistance to Fusarium head blight of wheat in China. In: Leonard KJ, Bushnell WR (eds) Fusarium head blight of wheat and barley. APS Press, St. Paul, pp 286-317 Ban T, Kishii M, Ammar K et al (2005) CIMMYT's challenges for global communication and germplasm enhancement for FHB resistance. In: Canty SM, Boring T, Wardwell J, Siler

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	Kianian SF, Cai XW (2007) Saturation and comparative	Guidance for Industry and FDA (2010) Advisory levels for deoxy-
	mapping of a major Fusarium head blight resistance QTL	nivalenol (DON) in finished wheat products for human con-
	in tetraploid wheat. Mol Breed 19:113-124	sumption and grains and grain by-products used for animal
	Chen S, Huang Z, Dai Y, Qin S, Gao Y, Zhang L, Gao Y, Chen J	feed. http://www.fda.gov/Food/GuidanceRegulation/Guidance
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	Cirlini M, Generotti S, Dall'Erta A, Lancioni P, Ferrazzano G,	Huhn M, Elias E, Ghavami F, Kianian S, Chao S, Zhong S,
	Massi A, Galaverna G, Dall'Asta C (2014) Durum wheat	Alamri M, Yahyaoui A, Mergoum M (2012) Tetraploid
	(Triticum durum Desf.) lines show different abilities to	Tunisian wheat germplasm as a new source of Fusarium
	form masked mycotoxins under greenhouse conditions.	head blight resistance. Crop Sci 52:136-145
	Toxins 6:81-95	Jauhar P (2014) Durum wheat genetic stocks involving chro-
	Clarke J, Clarke F, Pozniak C (2010) Forty-six years of genetic	mosome 1E of diploid wheatgrass: resistance to Fusarium
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	Plant Sci 90:791-801	Kishii M, Ban T, Ammar K (2005) Improvement of FHB
	Commission Regulation (EC) No. 1126/2007 of 28 September	resistance of durum wheat. In: Canty SM, Boring T,
	2007 amending regulation (EC) No. 1881/2006 setting	Wardwell J, Siler L, Ward RW (eds) Proceedings of the
	maximum levels for certain contaminants in foodstuffs as	2005 national fusarium head blight forum, Milwaukee, WI,
	regards Fusarium toxins in maize and maize products (2007).	11-13 Dec. Michigan State University, East Lansing, p 52
	http://eur-lex.europa.eu/LexUriServ/LexUriServ.do?uri=OJ:	Krska R, Schubert-Ullrich P, Molinelli A, Sulyok M, Macdon-
	L:2007:255:0014:01:EN:HTML. (Accessed 27 July 2014)	ald S, Crews C (2008) Mycotoxin analysis: an update. Food
	Cuthbert PA, Somers DJ, Brule-Babel A (2007) Mapping of	Addit Contam Part A Chem Anal Control Expo Risk
	Fhb2 on chromosome 6BS: a gene controlling Fusarium	Assess 25(2):152-163
	head blight field resistance in bread wheat (Triticum aes-	Kumar S, Stack R, Friesen T, Faris J (2007) Identification of a
	tivum L.). Theor Appl Genet 114:429-437	novel Fusarium head blight resistance quantitative trait
	Dall'Asta C, Dall'Erta A, Mantovani P, Massi A, Galaverna G	locus on chromosome 7A in tetraploid wheat. Phytopa-
	(2013) Occurrence of deoxynivalenol and deoxynivalenol-	thology 97:592-597
	3-glucoside in durum wheat. World Mycotoxin J 6:83-91	Lemmens M, Scholz U, Berthiller F, Dall'Asta C, Koutnik A,
	Elias EM, Manthey FA, Stack RW, Kianian SF (2005) Breeding	Schuhmacher R, Adam G, Buerstmayr H, Mesterhazy A,
	efforts to develop Fusarium head blight resistant durum	Krska R, Ruckenbauer P (2005) The ability to detoxify the
	wheat in North Dakota. In: Canty SM, Boring T, Wardwell	mycotoxin deoxynivalenol colocalizes with a major
	J, Siler L, Ward RW (eds) Proceedings of the 2005 national	quantitative trait locus for Fusarium head blight resistance
	fusarium head blight forum, Milwaukee, WI, 11-13 Dec.	in wheat. Mol Plant Microbe Interact 18:1318-1324
	Michigan State University, East Lansing, pp 25-26	Leonard KJ, Bushnell WR (2003) Fusarium head blight of wheat
	Fakhfakh MM, Yahyaoui A, Rezgui S, Elias EM, Daaloul A	and barley. APS Press, St. Paul
	(2011) Inheritances of Fusarium head blight resistance in a	Liu S, Zhang X, Pumphrey MO, Stack RW, Gill BS, Anderson
	cross involving local and exotic durum wheat cultivars.	JA (2006) Complex microcolinearity among wheat, rice,
	Crop Sci 51:2517-2524	and barley revealed by fine mapping of the genomic region
	Fu S, Lv Z, Qi B, Guo X, Li J, Liu B, Han F (2012) Molecular	harboring a major QTL for resistance to Fusarium head
	cytogenetic characterization of wheat-Thinopyrum	blight in wheat. Funct Integr Genomics 6:83-89
	elongatum addition, substitution and translocation lines	Ma HX, Bai GH, Zhang X, Lu WZ (2006) Main effects, epis-
	with a novel source of resistance to wheat Fusarium head	tasis, and environmental interactions of quantitative trait
	blight. J Genet Genomics 39:103-110	loci for Fusarium head blight resistance in a recombinant
	Fuentes RG, Mickelson HR, Busch RH, Dill-Macky R, Evans	inbred population. Phytopathology 96:534-541
	CK, Thompson WG, Wiersma JV, Xie W, Dong Y,	236-276 Maccaferri M, Cane MA, Salvi S, Noli E, Colalongo C, Massi A,
	Anderson JA (2005) Resource allocation and cultivar sta-	Buerstmayr M, Huber K, Heckmann J, Steiner B, Nelson JC, Clarke F, Pozniak C, Korol A, Fahima T, Dubcovsky J, Xu
	bility in breeding for Fusarium head blight resistance in	Buerstmayr H (2012b) Mapping of QTL for Fusarium head S, Karsai I, Knox R, Clarke J, Tuberosa R (2014a) A
	spring wheat. Crop Sci 45:1965-1972	blight resistance and morphological and developmental traits consensus framework map of durum wheat (Triticum
	Garvin D, Stack R, Hansen J (2009) Quantitative trait locus	in three backcross populations derived from Triticum dicoc-durum Desf.) suitable for linkage disequilibrium analysis
	mapping of increased Fusarium head blight susceptibility	cum 9 Triticum durum. Theor Appl Genet 125:1751-1765 and genome-wide association mapping. BMC Genom
	associated with a wild emmer wheat chromosome. Phyto-	Buerstmayr M, Alimari A, Steiner B, Buerstmayr H (2013) 15(1):873
	pathology 99:447-452	Genetic mapping of QTL for resistance to Fusarium head Maccaferri M, Ricci A, Salvi S, Milner SG, Noli E, Martelli PG,
	Ghavami F, Elias E, Mamidi S et al (2011) Mixed model	blight spread (type 2 resistance) in a Triticum dicocco-Casadio R, Ammar K, Blanco A, Desiderio F, Dubcovsky
	association mapping for Fusarium head blight resistance in	ides 9 Triticum durum backcross-derived population.
	tunisian-derived durum wheat populations. G3 1:209-218	Theor Appl Genet 126:2825-2834
	Gilbert J, Haber S (2013) Overview of some recent research	Cai X, Chen PD, Xu SS, Oliver RE, Chen X (2005) Utilization
	developments in Fusarium head blight of wheat. Can J	of alien genes to enhance Fusarium head blight resistance
	Plant Pathol 35:149-174	in wheat-a review. Euphytica 142:309-318

Anderson J, Stack R, Liu S, Waldron B, Fjeld A, Coyne C, Moreno-Sevilla B, Fetch J, Song Q, Cregan P, Frohberg R (2001) L, Ward RW (eds) Proceedings of the 2005 national fusarium head blight forum, Milwaukee, WI, 11-13 Dec. Michigan State University, East Lansing, pp 6-10 Berthiller F, Crews C, Dall'Asta C, De Saeger S, Haesaert G, Karlovsky P, Oswald IP, Seefelder W, Speijers G, Stroka J (2013) Masked mycotoxins: a review. Mol Nutr Food Res 57:165-186 Buerstmayr H, Lemmens M, Hartl L, Doldi L, Steiner B, Stierschneider M, Ruckenbauer P (2002) Molecular mapping of QTLs for Fusarium head blight resistance in spring wheat. I. Resistance to fungal spread (type II resistance). Theor Appl Genet 104:84-91 Buerstmayr H, Steiner B, Hartl L, Griesser M, Angerer N, Lengauer D, Miedaner T, Schneider B, Lemmens M (2003a) Molecular mapping of QTLs for Fusarium head blight resistance in spring wheat. II. Resistance to fungal penetration and spread. Theor Appl Genet 107:503-508 Buerstmayr H, Stierschneider M, Steiner B, Lemmens M, Griesser M, Nevo E, Fahima T (2003b) Variation for resistance to head blight caused by Fusarium graminearum in wild emmer (Triticum dicoccoides) originating from Israel. Euphytica 130:17-23 Buerstmayr H, Ban T, Anderson JA (2009) QTL mapping and marker-assisted selection for Fusarium head blight resistance in wheat: a review. Plant Breed 128:1-26 Buerstmayr H, Adam G, Lemmens M (2012a) Resistance to head blight caused by Fusarium spp. in wheat. In: Sharma I (ed) Disease resistance in wheat. CABI plant protection series, vol 1, 1st edn. CAB International, Wallingford, pp J, Fahima T, Faris J, Korol A, Massi A, Morgante M, Mastrangelo A, Pozniak C, Xu S, Tuberosa R (2014b) A high-density, SNP-based consensus map of tetraploid wheat as a bridge to integrate durum and bread wheat genomics and breeding. Plant Biotechnol J (in press)

  . A relatively small number of QTL mapping studies aimed at dissecting the genetic architecture of FHB resistance in tetraploid wheat to date, which have been recently reviewed by[START_REF] Prat | Current knowledge on resistance to Fusarium head blight in tetraploid wheat[END_REF].QTL descending from Triticum dicoccoides accessions Israel A, PI478742, Mt. Hermon#22, and Mt. Gerizim#36 have been identified on chromosomes 3A(Otto et al. 2002;[START_REF] Gladysz | Evaluation and genetic mapping of resistance to Fusarium head blight in Triticum dicoccoides[END_REF]

2007;

[START_REF] Chen | Saturation and comparative mapping of a major Fusarium head blight resistance QTL in tetraploid wheat[END_REF][START_REF] Buerstmayr | Genetic mapping of QTL for resistance to Fusarium head blight spread (type 2 resistance) in a Triticum dicoccoides × Triticum durum backcross-derived population[END_REF] Zhu et al. 2016b

), 4A

[START_REF] Gladysz | Evaluation and genetic mapping of resistance to Fusarium head blight in Triticum dicoccoides[END_REF]

), 6B

[START_REF] Buerstmayr | Genetic mapping of QTL for resistance to Fusarium head blight spread (type 2 resistance) in a Triticum dicoccoides × Triticum durum backcross-derived population[END_REF] 7A (Kumar et al. 2007)

. Triticum dicoccum accessions PI 41025, Td-161 and BGRC3487 provided resistance QTL on 3A, 3B, 4B, 5A, 6A, 6B, 7A and 7B

(Buerstmayr et al. 2012; Ruan et al. 2012; Zhang et al. 2014)

. Triticum carthlicum accession Blackbird contributed one resistance QTL mapping to 6B

(Somers et al. 2006

). The dissection of the genetic architecture of resistant T. durum Tunisian landraces by association mapping located a QTL on 3B

[START_REF] Ghavami | Mixed model association mapping for Fusarium head blight resistance in tunisianderived durum wheat populations[END_REF]

. In mapping studies based on crosses between susceptible durum cultivars and other resistant sources, a few resistance-conferring QTL alleles were contributed by the susceptible durum parents, notably those on chromosomes 2A, 2B, 3B and 5B from cultivars Ben

(Zhang et al. 2014)

, Strongfield

(Somers et al. 2006)

, Floradur

(Buerstmayr et al. 2012), and Lebsock (Ghavami et al. 2011), respectively.

Table 1

 1 Means of parents and mean, minimum and maximum values of populations, least significant differences at α < 0.05 (LSD 0.05 ) and broad-sense heritability coefficient (H 2 ) or repeatability of analyzed traits in field and greenhouse (GH) experiments

	Parents

Table 2

 2 Pearson correlation coefficients between FHB severity (AUDPC), plant height (cm) and flowering date (days after May 1st) for the overall means

Table 3

 3 Locations and estimates of QTL for FHB severity (AUDPC) using multiple QTL

	mapping
			Closest
	Population	Chr.	marker	Overall mean		2013		2014		2015
				Add a %PV b LOD c %PV b LOD c %PV b LOD %PV b LOD c
	KD	2BL 1072874	37	4.3	4.8	-	-	7.2	5.5	-	-
	DD	3BS 4410793	86	14.0	8.7	-	-	16.0	4.7	12.2	7.6
	KD	3BS Xbarc147 60	11.1	10.8	14.1	5.5	12.8	9.0	6.1	5.6
	SD	3BS Xbarc147 60	5.0	3.3	-	-	8.1	3.8	-	-
	SD	4AL 4541598	123	18.8	10.4	-	-	15.4	6.7	14.4	6.6
	DD	4BS RhtB1	156	38.4	18.6	18.8	6.0	26.0	7.1	55.5	23.1
	KD	4BS RhtB1	140	64.2	35.0	29.1	10.2	47.6 23.7 69.0	33.2
	SD	4BS RhtB1	126	19.4	10.7	-	-	10.3	4.7	16.0	7.2
	DD	5AL 1111359	59	6.2	4.3	15.0	5.0	-	-	-	-
	SD	6AS 4008755	139	24.9	12.9	28.0	6.9	24.6	9.8	25.4	10.6
	a Positive additive effects denote trait-increasing effect of the DBC-480 allele; additive effects were
	estimated as half the difference between phenotype averages for the homozygote

b Percentage of phenotypic variance explained by the QTL c LOD (logarithm of the odds) above LOD threshold at the 0.05 level of probability obtained through a 1,000-iteration permutation test

Table 4

 4 Locations and estimates of QTL for FHB spread (percent of infected spikelets PIS)

	using multiple QTL mapping
			Closest
	Experiment	Chr.	marker	Add a	%PV b	LOD c
	GH1	2A	1698827	-4.9	13.5	4.7
	GH1	3BS	Xbarc147	14.6	33.6	10.2
	GH2	3BS	1032004	4.9	14.6	3.8
	GH3	3BS	Xbarc147	4.7	10.3	3.0
	overall mean 3BS	Xbarc147	7.4	33.3	9.7
	GH3	4AL	1235993	-5.2	12.6	3.6
	a Positive additive effects denote trait-increasing effect of the DBC-480 allele; additive effects were
	estimated as half the difference between phenotype averages for the homozygote
	b Percentage of phenotypic variance explained by the QTL
	c LOD (logarithm of the odds) above LOD threshold at the 0.05 level of probability obtained through a
	1,000-iteration permutation test

Table 5

 5 Locations and estimates of QTL for plant height (cm) and flowering date (days after

	May 1 st ) using multiple QTL mapping
	Trait	Population chr	Closest marker	Add a	%PV b	LOD c
	Plant height	SD	4AL	4541598	-5.6	10.8	22.7
		KD	4BS	RhtB1	-17.4	95.4	74.4
		DD	4BS	RhtB1	-14.9	81.4	36.2
		SD	4BS	RhtB1	-11.0	37.0	45.8
		SD	6AS	4008755	-9.0	27.2	38.6
		SD	4BSx4AL		3.6	3.6	9.5
		SD	4BSx6AS		4.5	7.3	16.3
	Flowering date	DD	1BL	4009852	-0.3	6.9	3.6
		KD	2BS	1238155	0.3	11.6	5.0
		DD	2BS	4404789	0.8	44.3	16.8
		SD	2BS	988615	0.4	10.8	3.9
		SD	4AL	4541598	0.5	16.6	5.7
		KD	5AL	1148774	-0.6	37.8	13.6
		SD	6AS	4008755	0.5	20.4	6.8
		DD	6BS	1077913	0.3	7.1	3.7
	a Positive additive effects denote trait-increasing effect of the DBC-480 allele; additive effects
	were estimated as half the difference between phenotype averages for the homozygote
	b Percentage of phenotypic variance explained by the QTL

c LOD (logarithm of the odds) above LOD threshold at the 0.05 level of probability obtained through a 1,000-iteration permutation test

Génotypage de la population et construction des cartes de liaison

  . Pour chacune des populations, deux modèles ont été ajustés afin d'obtenir, pour chacun des caractères étudiés, le meilleur estimé linéaire non biaisé (BLUES ou « best linear unbiased estimates ») lors de l'analyse conjointe des essais (modèle 1) et au sein de chaque essai analysé individuellement (modèle 2). Une fois les cartes individuelles obtenues, les groupes de liaison ont été parent résistant DBC-480 et le parent lui-même, n'ont, cependant, pas été significatives. La pression de la maladie entre les expérimentations a été comparable, sauf en 2015 où davantage de symptômes ont été observés. L´héritabilité au sens large, calculée pour l'AUDPC est élevée au sein des trois populations (comprise entre 0,74 et 0,89). Dans chaque cas, la variance génotypique s´est avérée être plus élevée que les variances dues à l´interaction génotype x environnement et à la résiduelle. Un effet significatif du facteur génotype a également été mis en évidence par ANOVA pour tous les caractères étudiés.Afin d´évaluer la résistance de type 2 conférée par Fhb1, le pourcentage d´épillets infectés par épis (PIS) a été mesuré lors de trois essais en serre pour la population KD. Une héritabilité moyenne (H²=0,51) a été déterminée, bien que l´ANOVA ait montré un effet génotype significatif pour les 111 RILs évaluées. Des phénomènes de transgressions ont également été observés pour la résistance de type 2 bien que, de nouveau, les différences n'ont été significatives que pour les lignées très sensibles. Le parent DBC-480 a présenté moins de symptômes que le parent Karur avec des PIS respectifs de 18,3% et 38,4%. Des corrélations faibles mais néanmoins significatives ont pu être relevées entre la propagation et la sévérité (r=0,2, p<0,05). La période de floraison a présenté une distribution continue au sein des trois populations et cela bien qu´aucune différence significative n´ait pu être établie entre les parents. La sévérité de la maladie et la date de floraison ont été positivement corrélées pour la population SD, n´a pu être mise en évidence au cours de ce travail. Les QTL associés à la sévérité de la fusariose agissent donc principalement de manière additive.

	Analyse
	Modèle 1 :		où	est la valeur phénotypique, µ est
	la moyenne de la population, est l'effet du i ème génotype, est l'effet du j ème essai,	est
	l'effet de la k ème répétition au sein du j ème essai j,	est le ij ème effet de l'interaction
	génotype-par-essai et	la résiduelle. L'effet du génotype a été considéré comme fixe et tous les
	autres termes comme aléatoires.
	Modèle 2 :	où	est la valeur phénotypique, µ est la moyenne de la
	population, est l'effet du i ème génotype, L'effet du génotype a été également considéré comme fixe et la répétition comme aléatoire. est l'effet de la k ème répétition et la résiduelle. L'héritabilité au sens large de chaque caractère a été calculée selon l'équation ⁄ ⁄ ⁄ où est la variance génotypique, est la variance de l'interaction génotype-par-environnement, la variance de la résiduelle, m est le nombre d'essais et p le nombre total de répétition dans les différents essais (Holland et al. 2003). Le génotypage de la population a été réalisée à l'aide de marqueurs GBS (génotypage-par-séquençage ou « genotyping-by-sequencing ») développés par DArTseq. Un total de 7965, 4150 and 6235 marqueurs polymorphiques de haute qualité ont été utilisés pour la construction des Une faiblement et négativement corrélées pour KD et non corrélées pour DD. Néanmoins, au sein des
	cartes de liaison pour, respectivement, les populations KD, DD et SD. Le matériel végétal a de essais pris individuellement, aucune corrélation entre ces deux caractères n'a été observée en
	plus été génotypé avec les marqueurs moléculaires Xbarc147 (Song et al. 2005) et Xumn10 (Liu 2013 et 2015 pour la population KD, en 2013 et 2014 pour la population DD et en 2014 pour la
	et al. 2008), associés à Fhb1 ; et des marqueurs spécifiques pour les allèles de Rht-B1 (Ellis et al. population SD.

2002

). Les cartes de liaison ont été construites individuellement pour chacune des populations en utilisant l'algorithme MSTmap

[START_REF] Wu | Efficient and accurate construction of genetic linkage maps from the minimum spanning tree of a graph[END_REF]

inclus dans le paquet ASMap v0.4 (Taylor and Butler 2015) sous R. importante variation pour la hauteur des plantes (PH) a pu être observée dans les trois populations. Les parents sensibles Karur, Durobonus et SZD1029K ont été de 38 à 49 cm plus petits que le parent résistant DBC-480. Le caractère PH a présenté une distribution bimodale dans les populations KD et DD, et trimodale pour SD. Pour toutes les populations, la sévérité a été négativement corrélée à la hauteur des plantes, les individus les plus petits étant en moyenne plus sensibles à la fusariose. A l´inverse, aucune corrélation significative n´a pu être démontrée entre la résistance à la propagation de la fusariose après inoculation ponctuelle et la hauteur des plantes. épistatique

de QTL pour la propagation dans l'épi

  La détection de QTL menée dans la population KD a permis d´identifier un QTL sur le 3BS lié aux marqueursXbarc147et Xumn10. Il se trouve donc dans la même zone que le QTL de sévérité présenté précédemment et que Fhb1. L´allèle de résistance provient également du parent DBC-480. Ce QTL a été détecté systématiquement sur les trois essais réalisés en serre et également lors de l´analyse conjointe des essais. Il explique 33% de la variation phénotypique. Deux autres QTL ont été détectés sur le 2A et le 4AL mais seulement au sein d'un seul essai. Dans ces cas ci, l´allèle de résistance provenait du cultivar Karur.

Mol Breeding (2014) 34:1689-1699

Acknowledgements 1 Acknowledgements I would like to express my deepest gratitude and sincere appreciation to all people who have helped and supported me in the course of this project. It gives me immense pleasure to thank my supervisor at the BOKU University, Prof. Hermann Buerstmayr who gave me the chance to carry out this research project. I am thankful for his guidance, encouragements and careful suggestions which greatly helped me in the successful completion of my doctoral studies. My gratitude goes out to Dr. Thierry Langin, head of the research unit Genetics, Diversity and Ecophysiology of Cereals (UMR 1095 GDEC) in Clermont-Ferrand, who accepted to be part of this project. I greatly acknowledge his support and his trust in my work. I would like to express my heartfelt thanks to Dr. Olivier Robert who welcomed me in his team at Florimond-Desprez and has played a key role in encouraging and coordinating this whole project. His endless and warm support is sincerely acknowledged. I would like to thank the members of the reading committee Prof. Thomas Miedaner and Prof. Clay Sneller for generously offering their time and for their interest in reviewing this thesis. I am also grateful for Prof. Fiona Doohan and Prof. Dominique This who do me the honor of being part of the jury for the thesis defense. I would like to extend my deep gratitude to Dr. Wolfgang Schweiger and Dr. Barbara Steiner for their generous support and timely help throughout the duration of the project. I thank them for their scientific advice and insightful suggestions. I owe my sincere thanks to all the team of the Institute of Biotechnology in Plant Production. I thank Prof. Marc Lemmens for his insights in plant phytopathology, Maria Buerstmayr and Simone Zimmerl for their great help in the Lab, and Matthias Fidesser, Lisa-Maria Schmid and Theresia Köstlbauer for their support in setting up the experimental trials in Tulln. I remember the master's and bachelor's students Camille Guilbert, Ursa Prah and Elisabeth Wachter for their enthusiasm and tremendous help in collecting phenotypic and genotypic data. Acknowledgments We gratefully acknowledge financial support from the Austrian Science Fund (FWF), projects P17310-B05, and from the French Ministry of Higher Education and Research, CIFRE funding 2012/1405.

ACKNOWLEDGMENTS

We appreciate Marc Lemmens and Imer Maloku for providing Fusarium inoculum. We are grateful to Andrzej Kilian from DArT PL for giving us access to DArTseq consensus map. We thank Wolfgang Schweiger and Sebastian Michel for critically reviewing this manuscript. We acknowledge financial support from the French Ministry of Higher Education and Research, Conventions Industrielles de Formation par la REcherche (CIFRE) funding 2012/1405.

QTL analysis

Generation of linkage maps

7975, 4153 and 6242 polymorphic markers were generated from DARTseq and SSR marker data for the KD, DD and SD populations, respectively. Of these markers, 1064 were common across all three populations. The number of markers within maps for the KD, DD and SD populations was reduced to 1609, 1052 and 1006 unique loci, respectively. Total map lengths were 2806, 1781 and 2219 cM with an average marker distance of 1.9, 1.7 and 2.5 cM for the KD, DD and SD populations, respectively. Each linkage group could be unambiguously assigned to a chromosome based on the wheat DArTseq consensus map. Alignment to the consensus map showed low-coverage regions for the DD and SD populations on chromosomes 1A and 3A and on chromosomes 5A and 7A for the DD population. Despite that, all chromosomes were represented (Online Resource 3).

QTL analysis for FHB severity

QTL analysis conducted in individual populations identified a total of 6 genomic regions associated with FHB severity on chromosomes arms 2BL, 3BS, 4AL, 4BS, 5AL and 6AS (Table 3). The resistant parent DBC-480 contributed the resistance improving alleles at all loci. Linkage groups and confidence intervals of QTL are shown in Fig. 2. For reading ease, only selected markers at about 5 cM distances are displayed, while more detailed information including all mapped markers with their positions can be found in Online Resource 4. The two genomic regions on 3BS and 4BS were found repeatedly associated with FHB resistance at the same location in all three populations. The major QTL on 4BS co-localized with the Rht-B1 locus, which explained 64%, 38% and 19% of the total phenotypic variance in the KD, DD and SD population, respectively. On chromosome 3BS, the QTL mapped to marker positions Xbarc147 and Xumn10, which signposts the position of the introgressed Fhb1 and was detected for the analysis across experiments in all populations. The 3BS QTL was found consistently in all experiments for the KD population, while it was significant in two out of three experiments for the DD population and in one experiment for the SD population. The effects of the contrasting alleles at the Fhb1 and Rht-B1 loci, as well as the effect of allelic

Association between FHB resistance QTL and plant height QTL

The target genotype for a durum wheat breeder is a semi-dwarf plant type with improved FHB resistance. To investigate the feasibility of such an ideotype in our populations, we compared the effects of the detected FHB resistance QTL. In the SD population the three major resistance QTL mapping to Rht-B1, 4AL and 6AS overlapped with QTL for PH. The effect of Fhb1 -the only QTL not associated with PH in this population -does not efficiently counteract the increased susceptibility associated with the short-stemmed allele at the Rht-B1, 4AL and 6AS loci. In the KD and DD populations only the Rht-B1 locus contributed to both FHB severity and PH, while two other QTL, including Fhb1, were not associated with this morphological trait. To investigate the effects of allele combinations at the FHB resistance loci on FHB severity and PH, the RILs of each population were first classified in subgroups according to their allele status at the detected resistance QTL as illustrated in Fig 3 . The resistance level and average height were then compared among the different subgroups. In both populations, lines carrying the dwarfing allele Rht-B1b were significantly shorter and more susceptible than the ones harboring the wild type allele Rht-B1a. Plant height on average was reduced by 31% and 25% in the KD and DD Rht-B1b subpopulations, respectively, but the level of disease symptoms relative to Rht-B1a were about two-fold increased. In the KD population, lines carrying both resistance QTL at Fhb1 and 2BL loci in combination with Rht-B1b had between 22% to 38% less disease severity than the dwarf lines carrying one or no resistance QTL while showing equivalent levels of resistance as lines carrying Rht-B1a with no supplementary resistance QTL. In the DD population, the FHB resistance levels of dwarf lines carrying positive alleles at Fhb1 and 5AL were not significantly different from any Rht-B1a subpopulation while being 53% less diseased than dwarf lines with no resistance QTL.

Taken together, our findings demonstrate that the combination of 3BS+2BL QTL in the KD population and 3BS+5AL in the DD population efficiently offset the negative effect of Rht-B1b on FHB resistance.

AUTHORS CONTRIBUTIONS

NP performed the study and drafted the manuscript. CG, UP and EW helped collecting phenotypic data and genotyping of markers. BS carried out the initial crosses and developed the plant material used in this study. TL, OR and HB initiated the study and obtained funding.

Détection de QTL

L'analyse de QTL a été réalisée pour chaque caractère en utilisant les BLUES calculés au sein de chaque essai et pour les essais étudiés de manière conjointe, en utilisant le paquet R/qtl sous R (Broman et al. 2003). Les données manquantes ont été imputées en utilisant la méthode d'imputation de Sen and Churchill (2001). Les QTL ont été détectés via la régression de Haley-Knott en utilisant une analyse par intervalle et une analyse par intervalle composite. Le seuil de LOD pour l'existence de QTL a été calculé pour une erreur de type I à α=0.05 pour chaque caractère et pour chaque essai après un test basé sur 1000 permutations. Les QTL significatifs ont été intégrés dans un modèle QTL multiple. L'existence de QTL additionnels et la présence d'interaction entre QTL a ensuite été testée. Le modèle final établi a été comparé par ANOVA au modèle nul et le pourcentage de la variation phénotypique expliquée par chaque QTL, les effets additifs ainsi que les valeurs de LOD ont été estimés. Un intervalle de confiance a été défini pour chaque QTL en prenant pour chaque extrémité le LOD score maximum -1.5.

RESULTATS Variation et corrélations des caractères étudiés

L´évaluation du niveau d´infection par la fusariose a été mise en place sur trois populations biparentales inoculées artificiellement au champ. Cela a permis de déterminer les facteurs ayant un rôle significatif dans la diminution des effets de la maladie en conditions naturelles. Au cours

Analyse de QTL pour la sévérité de la fusariose

Les analyses QTL menées indépendamment sur les trois populations ont permis d´identifier six régions chromosomiques associées à la résistance à la fusariose sur les bras 2BL, 3BS, 4AL, 4BS, 5AL, et 6AS. Le parent résistant DBC-480 confère l'allèle de résistance à tous les loci détectés.

Les deux régions chromosomiques sur 3BS et 4BS sont associées à la résistance à la fusariose au sein des trois populations. Le QTL majeur sur 4BS co-localise avec le locus Rht-B1. Il explique 64%, 38% et 19% de la variance phénotypique totale au sein des populations KD, DD et SD. Le QTL identifié sur 3BS est lié aux marqueurs Xbarc147 et Xumn10, marqueurs qui signalent également le QTL de résistance introgressé Fhb1. Ce QTL présente un effet significatif pour la population KD lors de tous les essais, mais seulement pour deux essais sur trois pour la population DD et un essai sur trois pour la population SD. L'analyse révèle la présence d´autres QTL spécifiques à chacune des populations. Deux QTL majeurs ont été détectés chez SD sur les bras chromosomiques 4AL et le 6AS expliquant 19% et 25% de la variation phénotypique totale.

Ces deux QTL coïncident avec des QTL associés à la hauteur des plantes et à la date de floraison.

Dans la population DD, un QTL a été identifié sur 5AL lors de l'analyse conjointe des essais, où il explique 6% de la variation phénotypique. Ce QTL présente, en fait, un effet fort en 2013, où il explique 15% de cette variation, alors qu´il n'est pas détecté en 2014 et 2015. Dans la population KD, un QTL à effet faible a pu être détecté sur 2BL. Il explique 4% de la variance phénotypique, et est significatif en 2014 et lors de l´analyse conjointe de tous les essais. Aucune interaction

List of figures Introduction

List of tables Publication 1

Table 1 Information on mapping populations and the phenotyping methods performed for mapping Fusarium resistance QTL in tetraploid wheat…………………...………………27