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Calvin Bridges

Calvin Blackman Bridges (January 11, 1889 – December 27, 1938) was an American scientist known for his contributions to the field of genetics. Along with Alfred Sturtevant and H.J. Muller, Bridges was part of Thomas Hunt Morgan's famous "Fly Room" at Columbia University.

Early life
Calvin Blackman Bridges was born in Schuyler Falls, New York in 1889 to the parents of Leonard Bridges and Charlotte Blackman. Tragically, Calvin's mother died when he was two years old, and his father died a year later, leaving the young Calvin an orphan. Bridges was subsequently taken in and raised by his grandmother. It took Bridges several years to complete high school, graduating when he was 20 years old. Despite this setback, he moved on to be an outstanding student at Columbia University in New York City, which he attended both undergraduate and postgraduate school.

While taking a zoology class at Columbia, Bridges met Thomas Hunt Morgan. This started a relationship which would eventually lead to many important scientific discoveries regarding genetics and evolution.

Work and research
The "Fly Room" experiments began in 1910 and continued for seventeen years, with Thomas Hunt Morgan being the project's lead experimental developer. Among many others working alongside Bridges and Morgan in the laboratory were Alfred Sturtevant and Hermann Joseph Muller. The "Fly Room" experiments were the first to use the common fruit fly Drosophila melanogaster for research in genetics, because they are cheap, easily accessible, and reproduce quickly. The experiments resulted in many important early discoveries in the field, resolved previously unclear issues such as the organization of genetic information within chromosomes, chromosomal arrangement, and linkage in sex chromosomes, and contributed to the emergence of modern treatments of genetics and evolutionary biology from their classical foundations, all in an era before molecular biology had yet revealed the structure or nature of DNA. The group also contributed to the understanding of the impact of mutations on evolution in general. The success of the "Fly Room" experiments eventually made D. melanogaster a widely popular model organism for biological research of all types.

Bridges in particular was responsible for many improvements regarding the techniques and the equipment used in the experiments. He suggested the use binocular microscopes instead of hand lenses that had been using before, which improved data quality and convenience. Bridges also developed temperature controls for the experiments which proved to be more useful and yielded better results than the previous temperature controls.

Bridges published many works, one of his most famous being "Sex in Relation to Chromosomes and Genes". He also contributed many items to the Journal of Experimental Zoology and Science. His work with sex-linked traits suggested that chromosomes contained genes; Nettie Maria Stevens was later able to support this hypothesis by examining the chromosomes of the fruit flies. Bridges wrote a couple of papers presenting the proof. He thanked her as "Miss Stevens" without stating what her contribution was nor referring to her Ph.D.

Bridges' PhD thesis on "Non-disjunction as proof of the chromosome theory of heredity" appeared as the first paper in the first issue of the journal Genetics in 1916. In this paper, he also established that the Y chromosome does not determine gender in Drosophila. Bridges' best-known contribution among Drosophila researchers is his observation and documentation of the polytene chromosomes found in larval salivary gland cells. The banding patterns of these chromosomes are still used as genetic landmarks even by contemporary researchers. Bridges was elected to the National Academy of Sciences in 1936 for his work with Drosophila.

After his death, Bridges' student Katherine Brehme Warren completed work on The Mutants of Drosophila melanogaster (1944), a classic book which was for two decades an indispensable resource for geneticists, with information from the "Red Book" later being transferred to the FlyBase database. Morgan and Sturtevant destroyed almost all of Bridges' notebooks after his death, except the four which were not in their possession.

Personal life
Bridges married Gertrude Ives, with whom he had four children. He was known to be both brilliant and very kind and considerate, though he was equally well-known for his womanizing and his struggles to keep up with family obligations. He was an atheist. In 1938, Bridges died from what is believed to have been a case of syphilis.

title: Calvin Bridges


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Spin network

In physics, a spin network is a type of diagram which can be used to represent states and interactions between particles and fields in quantum mechanics. From a mathematical perspective, the diagrams are a concise way to represent multilinear functions and functions between representations of matrix groups. The diagrammatic notation can thus greatly simplify calculations.

Roger Penrose described spin networks in 1971. Spin networks have since been applied to the theory of quantum gravity by Carlo Rovelli, Lee Smolin, Jorge Pullin, Rodolfo Gambini and others.

Spin networks can also be used to construct a particular functional on the space of connections which is invariant under local gauge transformations.

Penrose's definition
A spin network, as described in Penrose (1971), is a kind of diagram in which each line segment represents the world line of a "unit" (either an elementary particle or a compound system of particles). Three line segments join at each vertex. A vertex may be interpreted as an event in which either a single unit splits into two or two units collide and join into a single unit. Diagrams whose line segments are all joined at vertices are called closed spin networks. Time may be viewed as going in one direction, such as from the bottom to the top of the diagram, but for closed spin networks the direction of time is irrelevant to calculations.

Each line segment is labelled with an integer called a spin number. A unit with spin number n is called an n-unit and has angular momentum nħ/2, where ħ is the reduced Planck constant. For bosons, such as photons and gluons, n is an even number. For fermions, such as electrons and quarks, n is odd.

Given any closed spin network, a non-negative integer can be calculated which is called the norm of the spin network. Norms can be used to calculate the probabilities of various spin values. A network whose norm is zero has zero probability of occurrence. The rules for calculating norms and probabilities are beyond the scope of this article. However, they imply that for a spin network to have nonzero norm, two requirements must be met at each vertex. Suppose a vertex joins three units with spin numbers a, b, and c. Then, these requirements are stated as: For example, a = 3, b = 4, c = 6 is impossible since 3 + 4 + 6 = 13 is odd, and a = 3, b = 4, c = 9 is impossible since 9 > 3 + 4. However, a = 3, b = 4, c = 5 is possible since 3 + 4 + 5 = 12 is even, and the triangle inequality is satisfied. Some conventions use labellings by half-integers, with the condition that the sum a + b + c must be a whole number.
 * Triangle inequality: a ≤ b + c and b ≤ a + c and c ≤ a + b.
 * Fermion conservation: a + b + c must be an even number.

Formal approach to definition
Formally, a spin network may be defined as a (directed) graph whose edges are associated with irreducible representations of a compact Lie group and whose vertices are associated with intertwiners of the edge representations adjacent to it.

Properties
A spin network, immersed into a manifold, can be used to define a functional on the space of connections on this manifold. One computes holonomies of the connection along every link (closed path) of the graph, determines representation matrices corresponding to every link, multiplies all matrices and intertwiners together, and contracts indices in a prescribed way. A remarkable feature of the resulting functional is that it is invariant under local gauge transformations.

In the context of loop quantum gravity
In loop quantum gravity (LQG), a spin network represents a "quantum state" of the gravitational field on a 3-dimensional hypersurface. The set of all possible spin networks (or, more accurately, "s-knots" – that is, equivalence classes of spin networks under diffeomorphisms) is countable; it constitutes a basis of LQG Hilbert space.

One of the key results of loop quantum gravity is quantization of areas: the operator of the area A of a two-dimensional surface Σ should have a discrete spectrum. Every spin network is an eigenstate of each such operator, and the area eigenvalue equals

 * $$A_{\Sigma} = 8\pi \ell_\text{PL}^2\gamma

\sum_i \sqrt{j_i(j_i+1)}$$

where the sum goes over all intersections i of Σ with the spin network. In this formula,
 * $\ell$PL is the Planck length,
 * $$\gamma$$ is the Immirzi parameter and
 * ji = 0, 1/2, 1, 3/2, ... is the spin associated with the link i of the spin network. The two-dimensional area is therefore "concentrated" in the intersections with the spin network.

According to this formula, the lowest possible non-zero eigenvalue of the area operator corresponds to a link that carries spin 1/2 representation. Assuming an Immirzi parameter on the order of 1, this gives the smallest possible measurable area of ~10−66 cm2.

The formula for area eigenvalues becomes somewhat more complicated if the surface is allowed to pass through the vertices, as with anomalous diffusion models. Also, the eigenvalues of the area operator A are constrained by ladder symmetry.

Similar quantization applies to the volume operator. The volume of a 3D submanifold that contains part of a spin network is given by a sum of contributions from each node inside it. One can think that every node in a spin network is an elementary "quantum of volume" and every link is a "quantum of area" surrounding this volume.

More general gauge theories
Similar constructions can be made for general gauge theories with a compact Lie group G and a connection form. This is actually an exact duality over a lattice. Over a manifold however, assumptions like diffeomorphism invariance are needed to make the duality exact (smearing Wilson loops is tricky). Later, it was generalized by Robert Oeckl to representations of quantum groups in 2 and 3 dimensions using the Tannaka–Krein duality.

Michael A. Levin and Xiao-Gang Wen have also defined string-nets using tensor categories that are objects very similar to spin networks. However the exact connection with spin networks is not clear yet. String-net condensation produces topologically ordered states in condensed matter.

Usage in mathematics
In mathematics, spin networks have been used to study skein modules and character varieties, which correspond to spaces of connections.

Early papers

 * I. B. Levinson, "Sum of Wigner coefficients and their graphical representation," Proceed. Phys-Tech Inst. Acad Sci. Lithuanian SSR 2, 17-30 (1956)
 * (see the Euclidean high temperature (strong coupling) section)
 * (see the sections on Abelian gauge theories)
 * (see the sections on Abelian gauge theories)

Modern papers

 * Xiao-Gang Wen, "Quantum Field Theory of Many-body Systems – from the Origin of Sound to an Origin of Light and Fermions," . (Dubbed string-nets here.)
 * Xiao-Gang Wen, "Quantum Field Theory of Many-body Systems – from the Origin of Sound to an Origin of Light and Fermions," . (Dubbed string-nets here.)
 * Xiao-Gang Wen, "Quantum Field Theory of Many-body Systems – from the Origin of Sound to an Origin of Light and Fermions," . (Dubbed string-nets here.)
 * Xiao-Gang Wen, "Quantum Field Theory of Many-body Systems – from the Origin of Sound to an Origin of Light and Fermions," . (Dubbed string-nets here.)
 * Xiao-Gang Wen, "Quantum Field Theory of Many-body Systems – from the Origin of Sound to an Origin of Light and Fermions," . (Dubbed string-nets here.)
 * Xiao-Gang Wen, "Quantum Field Theory of Many-body Systems – from the Origin of Sound to an Origin of Light and Fermions," . (Dubbed string-nets here.)

Books

 * G. E. Stedman, Diagram Techniques in Group Theory, Cambridge University Press, 1990.
 * Predrag Cvitanović, Group Theory: Birdtracks, Lie's, and Exceptional Groups, Princeton University Press, 2008.

license: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/4.0/

title: Spin network


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MG cars

MG is a British automotive marque founded by Cecil Kimber in the 1920s, and M.G. Car Company Limited was the British sports car manufacturer existing between 1930 and 1972 that made the marque well known. Since 2007, the marque is controlled by Chinese state-owned automaker SAIC Motor.

MG cars had their roots in a 1920s sales promotion sideline of Morris Garages, a retail sales and service centre in Oxford belonging to William Morris. The business's manager, Cecil Kimber, modified standard production Morris Oxfords and added MG Super Sports to the plate at the nose of the car. A separate M.G. Car Company Limited was incorporated in July 1930. It remained Morris's personal property until 1 July 1935, when he sold it to his holding company, Morris Motors Limited.

MG underwent many changes in ownership over the years. Morris's Nuffield Organization merged with Austin to create the British Motor Corporation Limited (BMC) in 1952. Its activities were renamed MG Division of BMC in 1967, and so it was a component of the 1968 merger that created British Leyland Motor Corporation (BLMC). The MG marque continued to be used by the successors of BLMC: British Leyland, the Rover Group and, by the start of 2000, the MG Rover Group, which entered receivership in 2005. The MG marque along with other assets of MG Rover were purchased by Nanjing Automobile Group (which merged into SAIC Motor in 2007). Production of MG vehicles restarted in 2007 in China under Chinese ownership. The first new MG model in the UK for 16 years, the MG6, was launched on 26 June 2011.

M.G. Car Company (1930–1972)

William Morris's Morris Garages in Longwall Street, Oxford, was the Oxford agent for his Morris cars. Cecil Kimber joined the dealership as its sales manager in 1921 and was promoted to general manager in 1922. Kimber began promoting sales by producing his own special versions of Morris cars.

Debate remains as to when MG car production started, although the first cars, rebodied Morris models that used coachwork from Carbodies of Coventry and known as "Kimber Specials", bore both Morris and MG badges. Reference to MG with the octagon badge appears in an Oxford newspaper from November 1923, and the MG Octagon was registered as a trademark by Morris Garages on 1 May 1924. Morris Garages assembled its cars in premises in Alfred Lane, Oxford. Demand soon caused a move to larger premises in Bainton Road in September 1925, sharing space with the Morris radiator works. Continuing expansion meant another move in 1927 to a separate factory in Edmund Road, Cowley, Oxford, near the main Morris factory, and for the first time, it was possible to include a production line.

In 1928, the company had become large enough to warrant an identity separate from the original Morris Garages, and The M.G. Car Company was used from March of that year. In October, for the first time, a stand was taken at the London Motor Show. Space soon ran out again, and a search for a permanent home led to the lease of part an old leather factory in Abingdon, Oxfordshire, in 1929. A limited liability company named M.G. Car Company was incorporated on 21 July 1930.

Kimber stayed with the company until 1941, when he fell out with Morris over procuring wartime work and was summarily dismissed. Kimber was tragically killed in the February 1945 King's Cross railway accident.

Under the Nuffield Organization
William Morris owned MG personally, and in a re-arrangement of his various personal holdings, he sold MG in 1935 to Morris Motors (itself the leading member of his Morris Organisation, later called the Nuffield Organization).

Under the British Motor Corporation (BMC)
The M.G. Car Company Limited was absorbed along with Morris into The British Motor Corporation Limited (BMC), created in 1952 as a merger of Morris Motors Limited and The Austin Motor Company Limited. Long-time service manager John Thornley took over as general manager, guiding the company through its best years until his retirement in 1969. Under BMC, several MG models were no more than badge-engineered versions of other marques, with the main exception being the small MG sports cars. BMC merged with Jaguar Cars in September 1966, and that December, the new company was named British Motor Holdings (BMH). BMH merged with the Leyland Motor Corporation in 1968 to form British Leyland Motor Corporation (BLMC).

Under British Leyland Motor Corporation (BLMC)
By this point, MG was nothing more than a marque used by BLMC, and from about 1972, the name "M.G. Car Company Limited" ceased to be used.

MG marque
The marque name originated from the initials of Morris Garages, William Morris's private retail sales and service company. The marque was in continuous use, except for the duration of the Second World War, from its inception in 1924 until 2005, and then from 2007 under Chinese ownership.

In the beginning, the marque was used predominantly for two-seater sports cars made at the M.G Car Company factory in Abingdon, some 10 mi south of Oxford.

Under British Leyland (1968–1990)
Following partial nationalisation in 1975, BLMC became British Leyland (later just BL). British Leyland's management and engineering staff were predominantly from the former Leyland organisation, which included MG's historical close rival Triumph. Triumph was grouped into BL's Specialist Division, alongside Rover and Jaguar, while MG was retained with the other former BMC marques in the Austin-Morris Division, which otherwise made mass-production family cars. While new Triumph models such as the TR7 and the Dolomite were launched during the 1970s, no new MG models were introduced apart from the limited-production V8 version of the MGB. While the MG operations was profitable these profits were entirely offset by the huge losses accrued by the rest of the Austin-Morris division and any funding to the Division within BL was allocated to urgently required mass market models, leaving MG with limited resources to develop and maintain its existing model range, which became increasingly outdated. Amidst a mix of economic, internal and external politics, the Abingdon factory was shut down on 24 October 1980 as part of the drastic programme of cutbacks necessary to turn BL around after the turbulent times of the 1970s. The last car built there was the MGB, and after the closure of the Abingdon plant, the MG marque was temporarily abandoned, and BL decided that there would be no immediate direct successor to the MGB or Midget.

Between 1982 and 1991, the MG marque used to badge-engineer sportier versions of Austin Rover's Metro, Maestro, and Montego ranges. The MG marque was not revived in its own right until 1992, with the MG RV8 – an updated MGB Roadster with a Rover V8 engine, which was previewed at the 1992 Birmingham Motor Show, with low-volume production commencing in 1993.

Under Rover Group (1992–2000)
After BL became the Rover Group in 1986, ownership of the MG marque passed to British Aerospace in 1988 and then in 1994 to BMW. The MG name was revived for a second time in 1992 with the launch of the MG RV8, followed by the mid-engined MG F in 1995, which proved to be more successful than the short-lived RV8.

Under MG Rover (2000–2006)
BMW sold the business in 2000 and the MG marque passed to the MG Rover Group based in Longbridge, Birmingham. The practice of selling unique MG sports cars alongside badge-engineered models (by now Rovers) continued. The Group went into receivership in 2005 and car production was suspended on 7 April 2005. As of 2003, the site of the former Abingdon factory was host to McDonald's and the Thames Valley Police with only the former office block still standing. The headquarters of the MG Car Club (established 1930) is situated next door.

In 2006, it was reported that an initiative called Project Kimber, led by David James, had entered talks with Nanjing to buy the MG brand to produce a range of sports cars based on the discontinued Smart Roadster design by DaimlerChrysler. No agreement was reached, which resulted in the AC Cars marque being adopted for the new model, instead. The project appeared dormant by 2009, and was not pursued.

Under MG Motor (2006–present)
On 22 July 2005, Chinese manufacturer Nanjing Automobile Group purchased the rights to the MG brand along with other assets of the MG Rover Group, forming NAC MG UK Limited. In 2007, Nanjing Automobile was acquired by another Chinese manufacturer SAIC Motor, and NAC MG UK Limited was renamed MG Motor UK Limited in 2009. Since then, the MG brand has been controlled by SAIC as a division within the company's passenger vehicle branch.

The first all-new MG-branded model for 16 years, the MG6, was officially launched in June 2011, and was assembled in China and in UK at the Longbridge plant. In September 2016, MG Motor ended car production at the Longbridge plant. The company cites "improving production scale efficiencies" as the reason of the plant closure. Since then, MG vehicles had been imported from China into the UK.

Since the purchase of the brand, SAIC has designated MG as its main brand internationally. Since 2019, MG has been the largest single-brand car exporter from China. In 2023, 88 percent of its sales was from outside China. Aside from selling cars designed by parent company SAIC Motor for the MG brand, MG Motor also markets rebadged vehicles from SAIC such as Roewe and Maxus, and from corporate sibling SAIC-GM-Wuling.

The most popular MG Motor product in international markets is the MG ZS subcompact SUV, with a cumulative sales of 999,612 units. It is one of the most exported cars from China. In 2023, MG Motor introduced its first new roadster, the Cyberster electric vehicle, which went on sale in 2024.

Models
The earliest model, the 1924 MG 14/28 consisted of a new sporting body on a Morris Oxford chassis. This car model continued through several versions following the updates to the Morris. The first car that can be described as a new MG, rather than a modified Morris was the MG 18/80 of 1928, which had a purpose-designed chassis and the first appearance of the traditional vertical MG grille. A smaller car was launched in 1929 with the first of a long line of Midgets starting with the M-Type based on a 1928 Morris Minor chassis. MG established a name for itself in the early days of the sport of international automobile racing. Beginning before and continuing after World War II, MG produced a line of cars known as the T-Series Midgets, which, post-war, were exported worldwide, achieving greater success than expected. These included the MG TC, MG TD, and MG TF, all of which were based on the pre-war MG TB, and updated with each successive model. MG departed from its earlier line of Y-Type saloons and pre-war designs and released the MGA in 1955. The MGB was released in 1962 to satisfy demand for a more modern and comfortable sports car. In 1965 the fixed head coupé (FHC) followed: the MGB GT. With continual updates, mostly to comply with increasingly stringent United States emissions and safety standards, the MGB was produced until 1980. Between 1967 and 1969 a short-lived model called the MGC was released. The MGC was based on the MGB body, but with a larger (and heavier) six-cylinder engine, and somewhat worse handling. MG also began producing the MG Midget in 1961. The Midget was a re-badged and slightly restyled second-generation Austin-Healey Sprite. To the dismay of many enthusiasts, the 1974 MGB was the last model made with chrome bumpers due to new United States safety regulations; the 1974½ bore thick black rubber bumpers that some claimed ruined the lines of the car. In 1973, the MGB GT V8 was launched with the ex-Buick Rover V8 engine and was built until 1976. As with the MGB, the Midget design was frequently modified until the Abingdon factory closed in October 1980 and the last of the range was made. The badge was also applied to versions of BMC saloons including the BMC ADO16, (as the MG 1100, 1275 and 1300) which was also available as a Riley, but with the MG pitched as slightly more "sporty".

The marque lived on after 1980 under BL, being used on a number of Austin saloons including the Metro, Maestro, and Montego. In New Zealand, the MG badge even appeared on the late 1980s Montego estate, called the MG 2.0 Si Wagon. There was a brief competitive history with a mid-engined, six-cylinder version of the Metro. The MG Metro finished production in 1990 on the launch of a Rover-only model. The MG Maestro and MG Montego remained on sale until 1991, when Rover cut production of these models to concentrate on the more modern 200 Series and 400 Series. High performance Rover Metro, 200 and 400 GTi models had gone on sale in late 1989 and throughout 1990 as the MG version of the Metro was discontinued in 1990 and the versions of the Maestro and Montego were axed in 1991.

The Rover Group revived the two-seater with the MG RV8 in 1992. The all-new MG F went on sale in 1995, becoming the first mass-produced "real" MG sports car since the MGB ceased production in 1980.

Following the May 2000 purchase of the MG and Rover brands by the Phoenix Consortium and the forming of the new MG Rover Group, the MG range was expanded in the summer of 2001 with the introduction of three sports models based on the contemporary range of Rover cars. The MG ZR was based on the Rover 25, the MG ZS on the Rover 45, and the MG ZT/ZT-T on the Rover 75.

The MG Rover Group purchased Qvale, which had taken over development of the De Tomaso Bigua. This car, renamed the Qvale Mangusta and already approved for sale in the United States, formed the basis of the MG XPower SV, an "extreme" V8-engined sports car. It was revealed in 2002 and went on sale in 2004.

Motorsport
From its earliest days MGs have been used in competition and from the early 1930s a series of dedicated racing cars such as the 1931 C-Type and 1934 Q-type were made and sold to enthusiasts who received considerable company assistance. This stopped in 1935 when MG was formally merged with Morris Motors and the Competition Department closed down. A series of experimental cars had also been made allowing Captain George Eyston to take several world speed records. In spite of the formal racing ban, speed record attempts continued with Goldie Gardner exceeding 200 mi/h in the 1100 cc EX135 in 1939.

After the Second World War record-breaking attempts restarted with 500 cc and 750 cc records being taken in the late 1940s. A decision was also taken to return to racing and a team of MGAs was entered in the tragedy-laden 1955 24 Hours of Le Mans race, the best car achieving 12th place. The British Motor Corporation (BMC) competition department was also based at the Abingdon plant, producing many winning rally and race cars, until the Abingdon factory closed and MGB production ceased in the autumn of 1980.

Prior to the use of the Toyota Tundra silhouette in the Craftsman Truck Series, MG was reported as the last foreign brand used in NASCAR. It was driven in 1963 by Smokey Cook.

In 2001 MG re-launched their motor sport campaign to cover the 24 Hours of Le Mans (MG-Lola EX257), British Touring Car Championship (BTCC) (MG ZS), British and World Rally Championships and MG Independent British Rally Championship (MG ZR). The Le Mans team failed to win the endurance race in 2001 and 2002 and quit in 2003. MG Sport+Racing raced in the British Touring Car Championships with the MG ZS between 2001 and 2003 as a factory team. In 2004 WSR raced the MG ZS as a privateer team. After three years without a major sponsor, WSR teamed up with RAC in 2006 and the team was called Team RAC. In 2007 an MG ZR driven by BRC Stars Champion Luke Pinder won class N1 on Britain's round of the World Rally championship. Wales Rally GB. The MG British Rally Challenge still runs today despite the liquidation in 2005.

In 2004 plans to race in the Deutsche Tourenwagen Masters (DTM) with a heavily modified V8 powered ZT supertouring car were cancelled due to MG Rover's liquidation in April 2005.

In January 2012, MG Motor announced that it would enter the 2012 British Touring Car Championship through the newly established MG KX Momentum Racing team. In its debut season the team ran two MG6s driven by Jason Plato and Andy Neate. Jason ended the season in third place, with the car yet to find its foot in wet conditions.

The team returned in 2013 with Sam Tordoff driving, who performed well in his debut year having joined through the KX Academy scheme. Plato once again came third, with Tordoff sixth.

MG won the 2014 Manufacturer's Championship to break Honda's four-year reign. After just three years of competition, the MG6 GT sealed the title by 95 points at the season finale at Brands Hatch. Drivers Plato and Tordoff racked up seven wins and 20 podiums in the 30-race calendar. Plato finished the Driver's Championship in second place, behind Colin Turkington, while Tordoff finished seventh. In 2014, a third MG6 GT was on the grid, driven by Marc Hynes—also maintained by Triple Eight but in a new livery that didn't resemble the other two MG cars. MG came second in the Constructors Championship in 2015, with Andrew Jordan leading the MG team by finishing the season fifth.

General sources

 * Northey, Tom. "MG: A Great Sporting Name", in Ward, Ian, Executive Editor. World of Automobiles, Volume 12, pp. 1333–41. London: Orbis, 1974.

title: MG cars


text:
Talk:Lobe

"Note: A lobe is characterized by a localized maximum bounded by identifiable nulls."

This could use further elucidation. Could an expert please describe the terms "localized maximum" and "nulls" in some detail? One can certainly guess the meaning, but a quick paragraph about what these mean in practice would be helpful. --Rethunk

Shouldn't it be mentioned that often a lobule is a subdivision of a biger lobe (as opposed to the intependent small lobe) --Yarikoptic 19:44, 22 September 2006 (UTC)

title: Talk:Lobe


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Drosophila melanogaster

Drosophila melanogaster is a species of fly (an insect of the order Diptera) in the family Drosophilidae. The species is often referred to as the fruit fly or lesser fruit fly, or less commonly the "vinegar fly", "pomace fly", or "banana fly". In the wild, D. melanogaster are attracted to rotting fruit and fermenting beverages, and are often found in orchards, kitchens and pubs.

Starting with Charles W. Woodworth's 1901 proposal of the use of this species as a model organism, D. melanogaster continues to be widely used for biological research in genetics, physiology, microbial pathogenesis, and life history evolution. As of 2017, six Nobel Prizes have been awarded to drosophilists for their work using the insect.

Drosophila melanogaster is typically used in research owing to its rapid life cycle, relatively simple genetics with only four pairs of chromosomes, and large number of offspring per generation. It was originally an African species, with all non-African lineages having a common origin. Its geographic range includes all continents, including islands. D. melanogaster is a common pest in homes, restaurants, and other places where food is served.

Flies belonging to the family Tephritidae are also called "fruit flies". This can cause confusion, especially in the Mediterranean, Australia, and South Africa, where the Mediterranean fruit fly Ceratitis capitata is an economic pest.

Etymology
The term "Drosophila", meaning "dew-loving", is a modern scientific Latin adaptation from Greek words δρόσος, drósos, "dew", and φιλία, philía, "lover". The term "melanogaster" meaning "black-belly", comes from Ancient Greek μέλας, mélas, “black”, and γᾰστήρ, gastḗr, "belly".

Physical appearance

Wild type fruit flies are yellow-brown, with brick-red eyes and transverse black rings across the abdomen. The black portions of the abdomen are the inspiration for the species name (melanogaster = "black-bellied"). The brick-red color of the eyes of the wild type fly are due to two pigments: xanthommatin, which is brown and is derived from tryptophan, and drosopterins, which are red and are derived from guanosine triphosphate. They exhibit sexual dimorphism; females are about 2.5 mm long; males are slightly smaller with darker backs. Males are easily distinguished from females based on colour differences, with a distinct black patch at the abdomen, less noticeable in recently emerged flies, and the sex combs (a row of dark bristles on the tarsus of the first leg). Furthermore, males have a cluster of spiky hairs (claspers) surrounding the reproducing parts used to attach to the female during mating. Extensive images are found at FlyBase.

Drosophila melanogaster can be distinguished from related species by the following combination of features: gena ~1/10 diameter of eye at greatest vertical height; wing hyaline and with costal index 2.4; male protarsus with a single row of ~12 setae forming a sex comb; male epandrial posterior lobe small and nearly triangular; female abdominal tergite 6 with dark band running to its ventral margin; female oviscapt small, pale, without dorsodistal depression and with 12-13 peg-like outer ovisensilla.

Drosophila melanogaster flies can sense air currents with the hairs on their backs. Their eyes are sensitive to slight differences in light intensity and will instinctively fly away when a shadow or other movement is detected.

Lifecycle and reproduction

Under optimal growth conditions at 25 C, the D. melanogaster lifespan is about 50 days from egg to death. The developmental period for D. melanogaster varies with temperature, as with many ectothermic species. The shortest development time (egg to adult), 7 days, is achieved at 28 C. Development times increase at higher temperatures (11 days at 30 C) due to heat stress. Under ideal conditions, the development time at 25 C is 8.5 days, at 18 C it takes 19 days  and at 12 C it takes over 50 days. Under crowded conditions, development time increases, while the emerging flies are smaller. Females lay some 400 eggs (embryos), about five at a time, into rotting fruit or other suitable material such as decaying mushrooms and sap fluxes. Drosophila melanogaster is a holometabolous insect, so it undergoes a full metamorphosis. Their life cycle is broken down into 4 stages: embryo, larva, pupa, adult. The eggs, which are about 0.5 mm long, hatch after 12–15 hours (at 25 C). The resulting larvae grow for about 4 days (at 25 °C) while molting twice (into second- and third-instar larvae), at about 24 and 48 h after hatching. During this time, they feed on the microorganisms that decompose the fruit, as well as on the sugar of the fruit itself. The mother puts feces on the egg sacs to establish the same microbial composition in the larvae's guts that has worked positively for herself. Then the larvae encapsulate in the puparium and undergo a 4-day-long metamorphosis (at 25 °C), after which the adults eclose (emerge).

Drosophila melanogaster, commonly known as the fruit fly, has been a significant model organism in embryonic development research. Many of its genes that regulate embryonic development and their mechanisms of action have been crucial in understanding the fundamental principles of embryonic development regulation in many multicellular organisms, including humans. Here are some important genes regulating embryonic development in Drosophila melanogaster and their modes of action:

Maternal genes: These genes are encoded in the female fruit fly and are present in the early stages of embryo development. They determine the embryo's main features and early development. For example, the gene called Bicoid regulates the formation of the embryo's anterior end, and its absence leads to an embryo lacking a head.

Zygotic genes: These genes are activated in later stages of embryo development when the fruit fly embryo begins to produce its own genetic products. For example, the hunchback gene regulates the formation of segments in the embryo.

Homeotic genes: This gene family regulates segmentation and axial patterning in development. They act as regulatory factors that determine cell fate in embryonic development. For example, the gene called Antennapedia regulates the formation of anterior limbs in the embryo.

Morphogens: These are molecules that form gradients in embryonic development and regulate cell fate depending on their position in the gradient. For example, the Hedgehog morphogen regulates the differentiation of segments and segment identity in the fruit fly embryo.

These genes and their modes of action form a complex regulatory network that guides the embryonic development of Drosophila melanogaster. They influence cell differentiation, segment formation, and axial patterning in the embryo, ultimately leading to the development of a fully formed adult fruit fly.

Males perform a sequence of five behavioral patterns to court females. First, males orient themselves while playing a courtship song by horizontally extending and vibrating their wings. Soon after, the male positions himself at the rear of the female's abdomen in a low posture to tap and lick the female genitalia. Finally, the male curls his abdomen and attempts copulation. Females can reject males by moving away, kicking, and extruding their ovipositor. Copulation lasts around 15–20 minutes, during which males transfer a few hundred, very long (1.76 mm) sperm cells in seminal fluid to the female. Females store the sperm in a tubular receptacle and in two mushroom-shaped spermathecae; sperm from multiple matings compete for fertilization. A last male precedence is believed to exist; the last male to mate with a female sires about 80% of her offspring. This precedence was found to occur through both displacement and incapacitation. The displacement is attributed to sperm handling by the female fly as multiple matings are conducted and is most significant during the first 1–2 days after copulation. Displacement from the seminal receptacle is more significant than displacement from the spermathecae. Incapacitation of first male sperm by second male sperm becomes significant 2–7 days after copulation. The seminal fluid of the second male is believed to be responsible for this incapacitation mechanism (without removal of first male sperm) which takes effect before fertilization occurs. The delay in effectiveness of the incapacitation mechanism is believed to be a protective mechanism that prevents a male fly from incapacitating his own sperm should he mate with the same female fly repetitively. Sensory neurons in the uterus of female D. melanogaster respond to a male protein, sex peptide, which is found in semen. This protein makes the female reluctant to copulate for about 10 days after insemination. The signal pathway leading to this change in behavior has been determined. The signal is sent to a brain region that is a homolog of the hypothalamus and the hypothalamus then controls sexual behavior and desire. Gonadotropic hormones in Drosophila maintain homeostasis and govern reproductive output via a cyclic interrelationship, not unlike the mammalian estrous cycle. Sex peptide perturbs this homeostasis and dramatically shifts the endocrine state of the female by inciting juvenile hormone synthesis in the corpus allatum.

D. melanogaster is often used for life extension studies, such as to identify genes purported to increase lifespan when mutated. D. melanogaster is also used in studies of aging. Werner syndrome is a condition in humans characterized by accelerated aging. It is caused by mutations in the gene WRN that encodes a protein with essential roles in repair of DNA damage. Mutations in the D. melanogaster homolog of WRN also cause increased physiologic signs of aging, such as shorter lifespan, higher tumor incidence, muscle degeneration, reduced climbing ability, altered behavior and reduced locomotor activity.

Meiosis
Meiotic recombination in D. melanogaster appears to be employed in repairing damage in germ-line DNA as indicated by the findings that meiotic recombination is induced by the DNA damaging agents ultraviolet light and mitomycin C.

Females

Females become receptive to courting males about 8–12 hours after emergence. Specific neuron groups in females have been found to affect copulation behavior and mate choice. One such group in the abdominal nerve cord allows the female fly to pause her body movements to copulate. Activation of these neurons induces the female to cease movement and orient herself towards the male to allow for mounting. If the group is inactivated, the female remains in motion and does not copulate. Various chemical signals such as male pheromones often are able to activate the group.

Also, females exhibit mate choice copying. When virgin females are shown other females copulating with a certain type of male, they tend to copulate more with this type of male afterwards than naïve females (which have not observed the copulation of others). This behavior is sensitive to environmental conditions, and females copulate less in bad weather conditions.

Males
D. melanogaster males exhibit a strong reproductive learning curve. That is, with sexual experience, these flies tend to modify their future mating behavior in multiple ways. These changes include increased selectivity for courting only intraspecifically, as well as decreased courtship times.

Sexually naïve D. melanogaster males are known to spend significant time courting interspecifically, such as with D. simulans flies. Naïve D. melanogaster will also attempt to court females that are not yet sexually mature, and other males. D. melanogaster males show little to no preference for D. melanogaster females over females of other species or even other male flies. However, after D. simulans or other flies incapable of copulation have rejected the males' advances, D. melanogaster males are much less likely to spend time courting nonspecifically in the future. This apparent learned behavior modification seems to be evolutionarily significant, as it allows the males to avoid investing energy into futile sexual encounters.

In addition, males with previous sexual experience modify their courtship dance when attempting to mate with new females—the experienced males spend less time courting, so have lower mating latencies, meaning that they are able to reproduce more quickly. This decreased mating latency leads to a greater mating efficiency for experienced males over naïve males. This modification also appears to have obvious evolutionary advantages, as increased mating efficiency is extremely important in the eyes of natural selection.

Polygamy
Both male and female D. melanogaster flies act polygamously (having multiple sexual partners at the same time). In both males and females, polygamy results in a decrease in evening activity compared to virgin flies, more so in males than females. Evening activity consists of those in which the flies participate other than mating and finding partners, such as finding food. The reproductive success of males and females varies, because a female only needs to mate once to reach maximum fertility. Mating with multiple partners provides no advantage over mating with one partner, so females exhibit no difference in evening activity between polygamous and monogamous individuals. For males, however, mating with multiple partners increases their reproductive success by increasing the genetic diversity of their offspring. This benefit of genetic diversity is an evolutionary advantage because it increases the chance that some of the offspring will have traits that increase their fitness in their environment.

The difference in evening activity between polygamous and monogamous male flies can be explained with courtship. For polygamous flies, their reproductive success increases by having offspring with multiple partners, and therefore they spend more time and energy on courting multiple females. On the other hand, monogamous flies only court one female, and expend less energy doing so. While it requires more energy for male flies to court multiple females, the overall reproductive benefits it produces has kept polygamy as the preferred sexual choice.

The mechanism that affects courtship behavior in Drosophila is controlled by the oscillator neurons DN1s and LNDs. Oscillation of the DN1 neurons was found to be effected by sociosexual interactions, and is connected to mating-related decrease of evening activity.

Model organism in genetics
D. melanogaster remains one of the most studied organisms in biological research, particularly in genetics and developmental biology. It is also employed in studies of environmental mutagenesis.

History of use in genetic analysis
D. melanogaster was among the first organisms used for genetic analysis, and today it is one of the most widely used and genetically best-known of all eukaryotic organisms. All organisms use common genetic systems; therefore, comprehending processes such as transcription and replication in fruit flies helps in understanding these processes in other eukaryotes, including humans.

Thomas Hunt Morgan began using fruit flies in experimental studies of heredity at Columbia University in 1910 in a laboratory known as the Fly Room. The Fly Room was cramped with eight desks, each occupied by students and their experiments. They started off experiments using milk bottles to rear the fruit flies and handheld lenses for observing their traits. The lenses were later replaced by microscopes, which enhanced their observations. Morgan and his students eventually elucidated many basic principles of heredity, including sex-linked inheritance, epistasis, multiple alleles, and gene mapping.

D. melanogaster had historically been used in laboratories to study genetics and patterns of inheritance. However, D. melanogaster also has importance in environmental mutagenesis research, allowing researchers to study the effects of specific environmental mutagens.

Reasons for use in laboratories
There are many reasons the fruit fly is a popular choice as a model organism:
 * Its care and culture require little equipment, space, and expense even when using large cultures.
 * It can be safely and readily anesthetized (usually with ether, carbon dioxide gas, by cooling, or with products such as FlyNap).
 * Its morphology is easy to identify once anesthetized.
 * It has a short generation time (about 10 days at room temperature), so several generations can be studied within a few weeks.
 * It has a high fecundity (females lay up to 100 eggs per day, and perhaps 2000 in a lifetime).
 * Males and females are readily distinguished, and virgin females can be easily identified by their light-colored, translucent abdomen, facilitating genetic crossing.
 * The mature larva has giant chromosomes in the salivary glands called polytene chromosomes, "puffs", which indicate regions of transcription, hence gene activity. The under-replication of rDNA occurs resulting in only 20% of DNA compared to the brain. Compare to the 47%, less rDNA in Sarcophaga barbata ovaries.
 * It has only four pairs of chromosomes – three autosomes, and one pair of sex chromosomes.
 * Males do not show meiotic recombination, facilitating genetic studies.
 * Recessive lethal "balancer chromosomes" carrying visible genetic markers can be used to keep stocks of lethal alleles in a heterozygous state without recombination due to multiple inversions in the balancer.
 * The development of this organism—from fertilized egg to mature adult—is well understood.
 * Genetic transformation techniques have been available since 1987. One approach of inserting foreign genes into the Drosophila genome involves P elements. The transposable P elements, also known as transposons, are segments of bacterial DNA that are transferred into the fly genome. Transgenic flies have already contributed to many scientific advances, e.g., modeling such human diseases as Parkinson's, neoplasia, obesity, and diabetes.
 * Its complete genome was sequenced and first published in 2000.
 * Sexual mosaics can be readily produced, providing an additional tool for studying the development and behavior of these flies.

Genetic markers

Genetic markers are commonly used in Drosophila research, for example within balancer chromosomes or P-element inserts, and most phenotypes are easily identifiable either with the naked eye or under a microscope. In the list of a few common markers below, the allele symbol is followed by the name of the gene affected and a description of its phenotype. (Note: Recessive alleles are in lower case, while dominant alleles are capitalised.)
 * Cy1: Curly; the wings curve away from the body, flight may be somewhat impaired
 * e1: Ebony; black body and wings (heterozygotes are also visibly darker than wild type)
 * Sb1: Stubble; bristles are shorter and thicker than wild type
 * w1: White; eyes lack pigmentation and appear white
 * bw: Brown; eye color determined by various pigments combined.
 * y1: Yellow; body pigmentation and wings appear yellow, the fly analog of albinism

Classic genetic mutations
Drosophila genes are traditionally named after the phenotype they cause when mutated. For example, the absence of a particular gene in Drosophila will result in a mutant embryo that does not develop a heart. Scientists have thus called this gene tinman, named after the Oz character of the same name. Likewise changes in the Shavenbaby gene cause the loss of dorsal cuticular hairs in Drosophila sechellia larvae. This system of nomenclature results in a wider range of gene names than in other organisms.

 * b: black- The black mutation was discovered in 1910 by Thomas Hunt Morgan. The black mutation results in a darker colored body, wings, veins, and segments of the fruit fly's leg. This occurs due to the fly's inability to create beta-alanine, a beta amino acid. The phenotypic expression of this mutation varies based on the genotype of the individual; for example, whether the specimen is homozygotic or heterozygotic results in a darker or less dark appearance. This genetic mutation is x-linked recessive.
 * bw: brown- The brown eye mutation results from inability to produce or synthesize pteridine (red) pigments, due to a point mutation on chromosome II. When the mutation is homozygous, the pteridine pigments are unable to be synthesized because in the beginning of the pteridine pathway, a defective enzyme is being coded by homozygous recessive genes. In all, mutations in the pteridine pathway produces a darker eye color, hence the resulting color of the biochemical defect in the pteridine pathway being brown.
 * m: miniature- One of the first records of the miniature mutation of wings was also made by Thomas Hunt Morgan in 1911. He described the wings as having a similar shape as the wild-type phenotype. However, their miniature designation refers to the lengths of their wings, which do not stretch beyond their body and, thus, are notably shorter than the wild-type length. He also noted its inheritance is connected to the sex of the fly and could be paired with the inheritance of other sex-determined traits such as white eyes. The wings may also demonstrate other characteristics deviant from the wild-type wing, such as a duller and cloudier color. Miniature wings are 1.5x shorter than wild-type but are believed to have the same number of cells. This is due to the lack of complete flattening by these cells, making the overall structure of the wing seem shorter in comparison. The pathway of wing expansion is regulated by a signal-receptor pathway, where the neurohormone bursicon interacts with its complementary G protein-coupled receptor; this receptor drives one of the G-protein subunits to signal further enzyme activity and results in development in the wing, such as apoptosis and growth.
 * se: sepia- The eye color of the sepia mutant is sepia, a reddish-brown color. In wild-type flies, ommochromes (brown) and drosopterins (red) give the eyes the typical red color. The drosopterins are made via a pathway that involves a pyrimidodiazepine synthase, which is encoded on chromosome 3L. The gene has a premature stop codon in sepia flies, so that the flies cannot produce the pyrimidodiazepine synthase and thus no red pigment, so that the eyes stay sepia. The sepia allele is recessive and thus offspring from sepia flies and homozygous wild type flies, has red eyes. The sepia phenotype does not depend on the sex of the fly.
 * v: vermilion- The vermilion mutants cannot produce the brown ommochromes leaving the red drosopterins so that the eyes are vermilion colored (a radiant red) compared to a wild-type D. melanogaster. The vermilion mutation is sex-linked and recessive. The gene that is defect lies on the X chromosome. The brown ommochromes are synthesised from kynurenine, which is made from tryptophane. Vermilion flies cannot convert tryptophane into kynurenine and thus cannot make ommochromes, either. Vermilion mutants live longer than wild-type flies. This longer life span may be associated with the reduced amount of tryptophan converted to kynurenine in vermilion flies.

 * vg: vestigial- A spontaneous mutation, discovered in 1919 by Thomas Morgan and Calvin Bridges. Vestigial wings are those not fully developed and that have lost function. Since the discovery of the vestigial gene in Drosophila melanogaster, there have been many discoveries of the vestigial gene in other vertebrates and their functions within the vertebrates. The vestigial gene is considered to be one of the most important genes for wing formation, but when it becomes over expressed the issue of ectopic wings begin to form. The vestigial gene acts to regulate the expression of the wing imaginal discs in the embryo and acts with other genes to regulate the development of the wings. A mutated vestigial allele removes an essential sequence of the DNA required for correct development of the wings.
 * w: white- Drosophila melanogaster wild type typically expresses a brick red eye color. The white eye mutation in fruit flies is caused due to the absence of two pigments associated with red and brown eye colors; peridines (red) and ommochromes (brown). In January 1910, Thomas Hunt Morgan first discovered the white gene and denoted it as w. The discovery of the white-eye mutation by Morgan brought about the beginnings of genetic experimentation and analysis of Drosophila melanogaster. Hunt eventually discovered that the gene followed a similar pattern of inheritance related to the meiotic segregation of the X chromosome. He discovered that the gene was located on the X chromosome with this information. This led to the discovery of sex-linked genes and also to the discovery of other mutations in Drosophila melanogaster. The white-eye mutation leads to several disadvantages in flies, such as a reduced climbing ability, shortened life span, and lowered resistance to stress when compared to wild type flies. Drosophila melanogaster has a series of mating behaviors that enable them to copulate within a given environment and therefore contribute to their fitness. After Morgan's discovery of the white-eye mutation being sex-linked, a study led by Sturtevant (1915) concluded that white-eyed males were less successful than wild-type males in terms of mating with females. It was found that the greater the density in eye pigmentation, the greater the success in mating for the males of Drosophila melanogaster.
 * y: yellow- The yellow gene is a genetic mutation known as Dmel\y within the widely used data base called FlyBase. This mutation can be easily identified by the atypical yellow pigment observed in the cuticle of the adult flies and the mouth pieces of the larva. The y mutation comprises the following phenotypic classes: the mutants that show a complete loss of pigmentation from the cuticle (y-type) and other mutants that show a mosaic pigment pattern with some regions of the cuticle (wild type, y2-type). The role of the yellow gene is diverse and is responsible for changes in behaviour, sex-specific reproductive maturation and, epigenetic reprogramming. The y gene is an ideal gene to study as it is visibly clear when an organism has this gene, making it easier to understand the passage of DNA to offspring.

Genome
The genome of D. melanogaster (sequenced in 2000, and curated at the FlyBase database ) contains four pairs of chromosomes – an X/Y pair, and three autosomes labeled 2, 3, and 4. The fourth chromosome is relatively very small and therefore often ignored, aside from its important eyeless gene. The D. melanogaster sequenced genome of 139.5 million base pairs has been annotated and contains around 15,682 genes according to Ensemble release 73. More than 60% of the genome appears to be functional non-protein-coding DNA involved in gene expression control. Determination of sex in Drosophila occurs by the X:A ratio of X chromosomes to autosomes, not because of the presence of a Y chromosome as in human sex determination. Although the Y chromosome is entirely heterochromatic, it contains at least 16 genes, many of which are thought to have male-related functions.

There are three transferrin orthologs, all of which are dramatically divergent from those known in chordate models.

Similarity to humans
A March 2000 study by National Human Genome Research Institute comparing the fruit fly and human genome estimated that about 60% of genes are conserved between the two species. About 75% of known human disease genes have a recognizable match in the genome of fruit flies, and 50% of fly protein sequences have mammalian homologs. An online database called Homophila is available to search for human disease gene homologues in flies and vice versa.

Drosophila is being used as a genetic model for several human diseases including the neurodegenerative disorders Parkinson's, Huntington's, spinocerebellar ataxia and Alzheimer's disease. The fly is also being used to study mechanisms underlying aging and oxidative stress, immunity, diabetes, and cancer, as well as drug abuse.

Development
The life cycle of this insect has four stages: fertilized egg, larva, pupa, and adult.

Embryogenesis in Drosophila has been extensively studied, as its small size, short generation time, and large brood size makes it ideal for genetic studies. It is also unique among model organisms in that cleavage occurs in a syncytium. During oogenesis, cytoplasmic bridges called "ring canals" connect the forming oocyte to nurse cells. Nutrients and developmental control molecules move from the nurse cells into the oocyte. In the figure to the left, the forming oocyte can be seen to be covered by follicular support cells.

After fertilization of the oocyte, the early embryo (or syncytial embryo) undergoes rapid DNA replication and 13 nuclear divisions until about 5000 to 6000 nuclei accumulate in the unseparated cytoplasm of the embryo. By the end of the eighth division, most nuclei have migrated to the surface, surrounding the yolk sac (leaving behind only a few nuclei, which will become the yolk nuclei). After the 10th division, the pole cells form at the posterior end of the embryo, segregating the germ line from the syncytium. Finally, after the 13th division, cell membranes slowly invaginate, dividing the syncytium into individual somatic cells. Once this process is completed, gastrulation starts.

Nuclear division in the early Drosophila embryo happens so quickly, no proper checkpoints exist, so mistakes may be made in division of the DNA. To get around this problem, the nuclei that have made a mistake detach from their centrosomes and fall into the centre of the embryo (yolk sac), which will not form part of the fly.

The gene network (transcriptional and protein interactions) governing the early development of the fruit fly embryo is one of the best understood gene networks to date, especially the patterning along the anteroposterior (AP) and dorsoventral (DV) axes (See under morphogenesis).

The embryo undergoes well-characterized morphogenetic movements during gastrulation and early development, including germ-band extension, formation of several furrows, ventral invagination of the mesoderm, and posterior and anterior invagination of endoderm (gut), as well as extensive body segmentation until finally hatching from the surrounding cuticle into a first-instar larva.

During larval development, tissues known as imaginal discs grow inside the larva. Imaginal discs develop to form most structures of the adult body, such as the head, legs, wings, thorax, and genitalia. Cells of the imaginal disks are set aside during embryogenesis and continue to grow and divide during the larval stages—unlike most other cells of the larva, which have differentiated to perform specialized functions and grow without further cell division. At metamorphosis, the larva forms a pupa, inside which the larval tissues are reabsorbed and the imaginal tissues undergo extensive morphogenetic movements to form adult structures.

Developmental plasticity
Biotic and abiotic factors experienced during development will affect developmental resource allocation leading to phenotypic variation, also referred to as developmental plasticity. As in all insects, environmental factors can influence several aspects of development in Drosophila melanogaster. Fruit flies reared under a hypoxia treatment experience decreased thorax length, while hyperoxia produces smaller flight muscles, suggesting negative developmental effects of extreme oxygen levels. Circadian rhythms are also subject to developmental plasticity. Light conditions during development affect daily activity patterns in Drosophila melanogaster, where flies raised under constant dark or light are less active as adults than those raised under a 12-hour light/dark cycle.

Temperature is one of the most pervasive factors influencing arthropod development. In Drosophila melanogaster temperature-induced developmental plasticity can be beneficial and/or detrimental. Most often lower developmental temperatures reduce growth rates which influence many other physiological factors. For example, development at 25 °C increases walking speed, thermal performance breadth, and territorial success, while development at 18 °C increases body mass, wing size, all of which are tied to fitness. Moreover, developing at certain low temperatures produces proportionally large wings which improve flight and reproductive performance at similarly low temperatures (See acclimation).

While certain effects of developmental temperature, like body size, are irreversible in ectotherms, others can be reversible. When Drosophila melanogaster develop at cold temperatures they will have greater cold tolerance, but if cold-reared flies are maintained at warmer temperatures their cold tolerance decreases and heat tolerance increases over time. Because insects typically only mate in a specific range of temperatures, their cold/heat tolerance is an important trait in maximizing reproductive output.

While the traits described above are expected to manifest similarly across sexes, developmental temperature can also produce sex-specific effects in D. melanogaster adults.
 * Females- Ovariole number is significantly affected by developmental temperature in D. melanogaster. Egg size is also affected by developmental temperature, and exacerbated when both parents develop at warm temperatures (See Maternal effect). Under stressful temperatures, these structures will develop to smaller ultimate sizes and decrease a female's reproductive output. Early fecundity (total eggs laid in first 10 days post-eclosion) is maximized when reared at 25 °C (versus 17 °C and 29 °C) regardless of adult temperature. Across a wide range of developmental temperatures, females tend to have greater heat tolerance than males.
 * Males- Stressful developmental temperatures will cause sterility in D. melanogaster males; although the upper temperature limit can be increased by maintaining strains at high temperatures (See acclimation). Male sterility can be reversible if adults are returned to an optimal temperature after developing at stressful temperatures. Male flies are smaller and more successful at defending food/oviposition sites when reared at 25 °C versus 18 °C; thus smaller males will have increased mating success and reproductive output.

Sex determination
Drosophila flies have both X and Y chromosomes, as well as autosomes. Unlike humans, the Y chromosome does not confer maleness; rather, it encodes genes necessary for making sperm. Sex is instead determined by the ratio of X chromosomes to autosomes. Furthermore, each cell "decides" whether to be male or female independently of the rest of the organism, resulting in the occasional occurrence of gynandromorphs.

Three major genes are involved in determination of Drosophila sex. These are sex-lethal, sisterless, and deadpan. Deadpan is an autosomal gene which inhibits sex-lethal, while sisterless is carried on the X chromosome and inhibits the action of deadpan. An AAX cell has twice as much deadpan as sisterless, so sex-lethal will be inhibited, creating a male. However, an AAXX cell will produce enough sisterless to inhibit the action of deadpan, allowing the sex-lethal gene to be transcribed to create a female.

Later, control by deadpan and sisterless disappears and what becomes important is the form of the sex-lethal gene. A secondary promoter causes transcription in both males and females. Analysis of the cDNA has shown that different forms are expressed in males and females. Sex-lethal has been shown to affect the splicing of its own mRNA. In males, the third exon is included which encodes a stop codon, causing a truncated form to be produced. In the female version, the presence of sex-lethal causes this exon to be missed out; the other seven amino acids are produced as a full peptide chain, again giving a difference between males and females.

Presence or absence of functional sex-lethal proteins now go on to affect the transcription of another protein known as doublesex. In the absence of sex-lethal, doublesex will have the fourth exon removed and be translated up to and including exon 6 (DSX-M[ale]), while in its presence the fourth exon which encodes a stop codon will produce a truncated version of the protein (DSX-F[emale]). DSX-F causes transcription of Yolk proteins 1 and 2 in somatic cells, which will be pumped into the oocyte on its production.

Immunity
The D. melanogaster immune system can be divided into two responses: humoral and cell-mediated. The former is a systemic response mediated in large part through the toll and Imd pathways, which are parallel systems for detecting microbes. Other pathways including the stress response pathways JAK-STAT and P38, nutritional signalling via FOXO, and JNK cell death signalling are all involved in key physiological responses to infection. D. melanogaster has an organ called the "fat body", which is analogous to the human liver. The fat body is the primary secretory organ and produces key immune molecules upon infection, such as serine proteases and antimicrobial peptides (AMPs). AMPs are secreted into the hemolymph and bind infectious bacteria and fungi, killing them by forming pores in their cell walls or inhibiting intracellular processes. The cellular immune response instead refers to the direct activity of blood cells (hemocytes) in Drosophila, which are analogous to mammalian monocytes/macrophages. Hemocytes also possess a significant role in mediating humoral immune responses such as the melanization reaction.

The immune response to infection can involve up to 2,423 genes, or 13.7% of the genome. Although the fly's transcriptional response to microbial challenge is highly specific to individual pathogens, Drosophila differentially expresses a core group of 252 genes upon infection with most bacteria. This core group of genes is associated with gene ontology categories such as antimicrobial response, stress response, secretion, neuron-like, reproduction, and metabolism among others. Drosophila also possesses several immune mechanisms to both shape the microbiota and prevent excessive immune responses upon detection of microbial stimuli. For instance, secreted PGRPs with amidase activity scavenge and degrade immunostimulatory DAP-type PGN in order to block Imd activation.

Unlike mammals, Drosophila have innate immunity but lack an adaptive immune response. However, the core elements of this innate immune response are conserved between humans and fruit flies. As a result, the fruit fly offers a useful model of innate immunity for disentangling genetic interactions of signalling and effector function, as flies do not have to contend with interference of adaptive immune mechanisms that could confuse results. Various genetic tools, protocols, and assays make Drosophila a classical model for studying the innate immune system, which has even included immune research on the international space station.

JAK-STAT signalling
Multiple elements of the Drosophila JAK-STAT signalling pathway bear direct homology to human JAK-STAT pathway genes. JAK-STAT signalling is induced upon various organismal stresses such as heat stress, dehydration, or infection. JAK-STAT induction leads to the production of a number of stress response proteins including Thioester-containing proteins (TEPs), Turandots, and the putative antimicrobial peptide Listericin. The mechanisms through which many of these proteins act is still under investigation. For instance, the TEPs appear to promote phagocytosis of Gram-positive bacteria and the induction of the toll pathway. As a consequence, flies lacking TEPs are susceptible to infection by toll pathway challenges.

The cellular response to infection
Circulating hemocytes are key regulators of infection. This has been demonstrated both through genetic tools to generate flies lacking hemocytes, or through injecting microglass beads or lipid droplets that saturate hemocyte ability to phagocytose a secondary infection. Flies treated like this fail to phagocytose bacteria upon infection, and are correspondingly susceptible to infection. These hemocytes derive from two waves of hematopoiesis, one occurring in the early embryo and one occurring during development from larva to adult. However Drosophila hemocytes do not renew over the adult lifespan, and so the fly has a finite number of hemocytes that decrease over the course of its lifespan. Hemocytes are also involved in regulating cell-cycle events and apoptosis of aberrant tissue (e.g. cancerous cells) by producing Eiger, a tumor necrosis factor signalling molecule that promotes JNK signalling and ultimately cell death and apoptosis.

Behavioral genetics and neuroscience
In 1971, Ron Konopka and Seymour Benzer published "Clock mutants of Drosophila melanogaster", a paper describing the first mutations that affected an animal's behavior. Wild-type flies show an activity rhythm with a frequency of about a day (24 hours). They found mutants with faster and slower rhythms, as well as broken rhythms—flies that move and rest in random spurts. Work over the following 30 years has shown that these mutations (and others like them) affect a group of genes and their products that form a biochemical or biological clock. This clock is found in a wide range of fly cells, but the clock-bearing cells that control activity are several dozen neurons in the fly's central brain.

Since then, Benzer and others have used behavioral screens to isolate genes involved in vision, olfaction, audition, learning/memory, courtship, pain, and other processes, such as longevity.

Following the pioneering work of Alfred Henry Sturtevant and others, Benzer and colleagues used sexual mosaics to develop a novel fate mapping technique. This technique made it possible to assign a particular characteristic to a specific anatomical location. For example, this technique showed that male courtship behavior is controlled by the brain. Mosaic fate mapping also provided the first indication of the existence of pheromones in this species. Males distinguish between conspecific males and females and direct persistent courtship preferentially toward females thanks to a female-specific sex pheromone which is mostly produced by the female's tergites.

The first learning and memory mutants (dunce, rutabaga, etc.) were isolated by William "Chip" Quinn while in Benzer's lab, and were eventually shown to encode components of an intracellular signaling pathway involving cyclic AMP, protein kinase A, and a transcription factor known as CREB. These molecules were shown to be also involved in synaptic plasticity in Aplysia and mammals.

The Nobel Prize in Physiology or Medicine for 2017 was awarded to Jeffrey C. Hall, Michael Rosbash, Michael W. Young for their works using fruit flies in understanding the "molecular mechanisms controlling the circadian rhythm".

Male flies sing to the females during courtship using their wings to generate sound, and some of the genetics of sexual behavior have been characterized. In particular, the fruitless gene has several different splice forms, and male flies expressing female splice forms have female-like behavior and vice versa. The TRP channels nompC, nanchung, and inactive are expressed in sound-sensitive Johnston's organ neurons and participate in the transduction of sound. Mutating the Genderblind gene, also known as CG6070, alters the sexual behavior of Drosophila, turning the flies bisexual.

Flies use a modified version of Bloom filters to detect novelty of odors, with additional features including similarity of novel odor to that of previously experienced examples, and time elapsed since previous experience of the same odor.

Aggression
As with most insects, aggressive behaviors between male flies commonly occur in the presence of courting a female and when competing for resources. Such behaviors often involve raising wings and legs towards the opponent and attacking with the whole body. Thus, it often causes wing damage, which reduces their fitness by removing their ability to fly and mate.

Acoustic communication
In order for aggression to occur, male flies produce sounds to communicate their intent. A 2017 study found that songs promoting aggression contain pulses occurring at longer intervals. RNA sequencing from fly mutants displaying over-aggressive behaviors found more than 50 auditory-related genes (important for transient receptor potentials, Ca2+ signaling, and mechanoreceptor potentials) to be upregulated in the AB neurons located in Johnston's organ. In addition, aggression levels were reduced when these genes were knocked out via RNA interference. This signifies the major role of hearing as a sensory modality in communicating aggression.

Pheromone signaling
Other than hearing, another sensory modality that regulates aggression is pheromone signaling, which operates through either the olfactory system or the gustatory system depending on the pheromone. An example is cVA, an anti-aphrodisiac pheromone used by males to mark females after copulation and to deter other males from mating. This male-specific pheromone causes an increase in male-male aggression when detected by another male's gustatory system. However, upon inserting a mutation that makes the flies irresponsive to cVA, no aggressive behaviors were seen. This shows how there are multiple modalities for promoting aggression in flies.

Competition for food
Specifically, when competing for food, aggression occurs based on amount of food available and is independent of any social interactions between males. Specifically, sucrose was found to stimulate gustatory receptor neurons, which was necessary to stimulate aggression. However, once the amount of food becomes greater than a certain amount, the competition between males lowers. This is possibly due to an over-abundance of food resources. On a larger scale, food was found to determine the boundaries of a territory since flies were observed to be more aggressive at the food's physical perimeter.

Effect of sleep deprivation
However, like most behaviors requiring arousal and wakefulness, aggression was found to be impaired via sleep deprivation. Specifically, this occurs through the impairment of Octopamine and dopamine signaling, which are important pathways for regulating arousal in insects. Due to reduced aggression, sleep-deprived male flies were found to be disadvantaged at mating compared to normal flies. However, when octopamine agonists were administered upon these sleep-deprived flies, aggression levels were seen to be increased and sexual fitness was subsequently restored. Therefore, this finding implicates the importance of sleep in aggression between male flies.

Vision

The compound eye of the fruit fly contains 760 unit eyes or ommatidia, and are one of the most advanced among insects. Each ommatidium contains eight photoreceptor cells (R1-8), support cells, pigment cells, and a cornea. Wild-type flies have reddish pigment cells, which serve to absorb excess blue light so the fly is not blinded by ambient light. Eye color genes regulate cellular vesicular transport. The enzymes needed for pigment synthesis are then transported to the cell's pigment granule, which holds pigment precursor molecules.

Each photoreceptor cell consists of two main sections, the cell body and the rhabdomere. The cell body contains the nucleus, while the 100-μm-long rhabdomere is made up of toothbrush-like stacks of membrane called microvilli. Each microvillus is 1–2 μm in length and about 60 nm in diameter. The membrane of the rhabdomere is packed with about 100 million opsin molecules, the visual protein that absorbs light. The other visual proteins are also tightly packed into the microvilli, leaving little room for cytoplasm.

Opsins and spectral sensitivity

The genome of Drosophila encodes seven opsins, five of those are expressed in the omatidia of the eye. The photoreceptor cells R1-R6 express the opsin Rh1, which absorbs maximally blue light (around 480 nm), however the R1-R6 cells cover a broader range of the spectrum than an opsin would allow due to a sensitising pigment  that adds two sensitivity maxima in the UV-range (355 and 370 nm). The R7 cells come in two types with yellow and pale rhabdomeres (R7y and R7p). The pale R7p cells express the opsin Rh3, which maximally absorbs UV-light (345 nm). The R7p cells are strictly paired with the R8p cells that express Rh5, which maximally absorbs violet light (437 nm). The other, the yellow R7y cells express a blue-absorbing screening pigment and the opsin Rh4, which maximally absorbs UV-light (375 nm). The R7y cells are strictly paired with R8y cells that express Rh6, which maximally absorbs UV-light (508 nm). In a subset of omatidia both R7 and R8 cells express the opsin Rh3.

However, these absorption maxima of the opsins where measured in white eyed flies without screening pigments (Rh3-Rh6), or from the isolated opsin directly (Rh1). Those pigments reduce the light that reaches the opsins depending on the wavelength. Thus in fully pigmented flies, the effective absorption maxima of opsins differs and thus also the sensitivity of their photoreceptor cells. With screening pigment, the opsin Rh3 is short wave shifted from 345 nm to 330 nm and Rh4 from 375 nm to 355 nm. Whether screening pigment is present does not make a practical difference for the opsin Rh5 (435 nm and 437 nm), while the opsin R6 is long wave shifted by 92 nm from 508 nm to 600 nm.

Additionally of the opsins of the eye, Drosophila has two more opsins: The ocelli express the opsin Rh2, which maximally absorbs violet light (~420 nm). And the opsin Rh7, which maximally absorbs UV-light (350 nm) with an unusually long wavelength tail up to 500 nm. The long tail disappears if a lysine at position 90 is replaced by glutamic acid. This mutant then absorbs maximally violet light (450 nm). The opsin Rh7 entrains with cryptochrome the circadian rhythm of Drosophila to the day-night-cycle in the central pacemaker neurons.

Each Drosophila opsin binds the carotenoid chromophore 11-cis-3-hydroxyretinal via a lysine. This lysine is conserved in almost all opsins, only a few opsins have lost it during evolution. Opsins without it are not light sensitive. In particular, the Drosophila opsins Rh1, Rh4, and Rh7 function not only as photoreceptors, but also as chemoreceptors for aristolochic acid. These opsins still have the lysine like other opsins. However, if it is replaced by an arginine in Rh1, then Rh1 loses light sensitivity but still responds to aristolochic acid. Thus, the lysine is not needed for Rh1 to function as chemoreceptor.

Phototransduction
As in vertebrate vision, visual transduction in invertebrates occurs via a G protein-coupled pathway. However, in vertebrates, the G protein is transducin, while the G protein in invertebrates is Gq (dgq in Drosophila). When rhodopsin (Rh) absorbs a photon of light its chromophore, 11-cis-3-hydroxyretinal, is isomerized to all-trans-3-hydroxyretinal. Rh undergoes a conformational change into its active form, metarhodopsin. Metarhodopsin activates Gq, which in turn activates a phospholipase Cβ (PLCβ) known as NorpA.

PLCβ hydrolyzes phosphatidylinositol (4,5)-bisphosphate (PIP2), a phospholipid found in the cell membrane, into soluble inositol triphosphate (IP3) and diacylglycerol (DAG), which stays in the cell membrane. DAG, a derivative of DAG, or PIP2 depletion cause a calcium-selective ion channel known as transient receptor potential (TRP) to open and calcium and sodium flows into the cell. IP3 is thought to bind to IP3 receptors in the subrhabdomeric cisternae, an extension of the endoplasmic reticulum, and cause release of calcium, but this process does not seem to be essential for normal vision.

Calcium binds to proteins such as calmodulin (CaM) and an eye-specific protein kinase C (PKC) known as InaC. These proteins interact with other proteins and have been shown to be necessary for shut off of the light response. In addition, proteins called arrestins bind metarhodopsin and prevent it from activating more Gq. A sodium-calcium exchanger known as CalX pumps the calcium out of the cell. It uses the inward sodium gradient to export calcium at a stoichiometry of 3 Na+/ 1 Ca++.

TRP, InaC, and PLC form a signaling complex by binding a scaffolding protein called InaD. InaD contains five binding domains called PDZ domain proteins, which specifically bind the C termini of target proteins. Disruption of the complex by mutations in either the PDZ domains or the target proteins reduces the efficiency of signaling. For example, disruption of the interaction between InaC, the protein kinase C, and InaD results in a delay in inactivation of the light response.

Unlike vertebrate metarhodopsin, invertebrate metarhodopsin can be converted back into rhodopsin by absorbing a photon of orange light (580 nm).

About two-thirds of the Drosophila brain is dedicated to visual processing. Although the spatial resolution of their vision is significantly worse than that of humans, their temporal resolution is around 10 times better.

Grooming
Drosophila are known to exhibit grooming behaviors that are executed in a predictable manner. Drosophila consistently begin a grooming sequence by using their front legs to clean the eyes, then the head and antennae. Using their hind legs, Drosophila proceed to groom their abdomen, and finally the wings and thorax. Throughout this sequence, Drosophila periodically rub their legs together to get rid of excess dust and debris that accumulates during the grooming process.

Grooming behaviors have been shown to be executed in a suppression hierarchy. This means that grooming behaviors that occur at the beginning of the sequence prevent those that come later in the sequence from occurring simultaneously, as the grooming sequence consists of mutually exclusive behaviors. This hierarchy does not prevent Drosophila from returning to grooming behaviors that have already been accessed in the grooming sequence. The order of grooming behaviors in the suppression hierarchy is thought to be related to the priority of cleaning a specific body part. For example, the eyes and antennae are likely executed early on in the grooming sequence to prevent debris from interfering with the function of D. melanogaster's sensory organs.

Walking
Like many other hexapod insects, Drosophila typically walk using a tripod gait. This means that three of the legs swing together while the other three remain stationary, or in stance. Specifically, the middle leg moves in phase with the contralateral front and hind legs. However, variability around the tripod configuration exists along a continuum, meaning that flies do not exhibit distinct transitions between different gaits. At fast walking speeds, the walking configuration is mostly tripod (3 legs in stance), but at slower walking speeds, flies are more likely to have four (tetrapod) or five legs in stance (wave). These transitions may help to optimize static stability. Because flies are so small, inertial forces are negligible compared with the elastic forces of their muscles and joints or the viscous forces of the surrounding air.

Flight
Flies fly via straight sequences of movement interspersed by rapid turns called saccades. During these turns, a fly is able to rotate 90° in less than 50 milliseconds.

Characteristics of Drosophila flight may be dominated by the viscosity of the air, rather than the inertia of the fly body, but the opposite case with inertia as the dominant force may occur. However, subsequent work showed that while the viscous effects on the insect body during flight may be negligible, the aerodynamic forces on the wings themselves actually cause fruit flies' turns to be damped viscously.

Connectome
Drosophila is one of the few animals (C. elegans being another) where detailed neural circuits (a connectome) are available.

A high-level connectome, at the level of brain compartments and interconnecting tracts of neurons, exists for the full fly brain. A version of this is available online.

Detailed circuit-level connectomes exist for the lamina and a medulla column, both in the visual system of the fruit fly, and the alpha lobe of the mushroom body.

In May 2017 a paper published in bioRxiv presented an electron microscopy image stack of the whole adult female brain at synaptic resolution. The volume is available for sparse tracing of selected circuits. Since then, multiple datasets have been collected including a dense connectome of half the central brain of Drosophila in 2020, and a dense connectome of the entire female adult nerve cord in 2021. Generally, these datasets are acquired by sectioning the tissue (e.g. the brain) into thin sections (on order of ten or hundreds of nanometers). Each section is then imaged using an electron microscope and these images are stitched and aligned together to create a 3D image volume. The methods used in reconstruction and initial analysis of the such datasets followed. Due to advancements in deep learning, automated methods for image segmentation have made large scale reconstruction providing dense reconstructions of all the neurites within the volume. Furthermore, the resolution of electron microscopy illuminates ultrastructural variations between neurons as well as the location of individual synapses, thereby providing a wiring diagram of synaptic connectivity between all neurites within the given dataset.

In 2023, the complete map of a Drosophila larval brain at the synapse level, and an analysis of its architecture was published. The larval brain consists of 3016 neurons and 548,000 synaptic sites, whereas the adult brain has about 150,000 neurons and 150 million synapses.

Misconceptions
Drosophila is sometimes referred to as a pest due to its tendency to live in human settlements where fermenting fruit is found. Flies may collect in homes, restaurants, stores, and other locations. The name and behavior of this species of fly have led to the misconception that it is a biological security risk in Australia and elsewhere. While other "fruit fly" species do pose a risk, D. melanogaster is attracted to fruit that is already rotting, rather than causing fruit to rot.

title: Drosophila melanogaster


text:
Donald Becker

Donald Becker is an American computer programmer who wrote Ethernet drivers for the Linux operating system.

Becker, in collaboration with Thomas Sterling, created the Beowulf clustering software while at NASA, to connect many inexpensive PCs to solve complex math problems typically reserved for classic supercomputers. For this work, Becker received the Gordon Bell Prize in 1997.

Becker became the Chief Technology Officer (CTO) of Scyld Computer Corporation, a wholly owned subsidiary of Penguin Computing, a developer and supplier of Beowulf clusters.

title: Donald Becker