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Talk:Equine coat color genetics

Comment
the following link has the most informative and easy-to-understand explanation of equine color genetics that I have come across: http://www.equinecolor.com/color.html

 * I would in turn suggest to include the following link because it is very easy to understand for beginners and gives a feel for how genetics work: http://www.jenniferhoffman.net/horse/equinegenetics.html --Xaya 13:04, 14 September 2011 (UTC) — Preceding unsigned comment added by 213.221.214.166 (talk)

 * It's a for-profit site, is slow to load, and is just pictures. Cute, but not really a RS by WP standards.   Montanabw (talk) 18:18, 14 September 2011 (UTC)

Recent Edit
I have revamped the page. It still needs work, and especially pictures inserted to make the concepts clearer. The curent version is based on http://dreamviewfarm.com/genetics.html. As author of that site, anyone wanting to take the time to copy the pics from there to here is welcome to.

Accuracy of article (Comment recently restored)
I have recently been researching the genetics of horses, and have found this article to be one of the least accurate I have come across. Although much of it is correct, it still states many theories that have been disproven for as long as a decade in some cases. I am currently writing an article on current horse genetics, and will post it here once it is complete. In the meantime, anyone researching horse genetics is recommended looking elsewhere. Bill Killed The Unicorns 08:01, 16 September 2006 (UTC)
 * Don't just slam, provide some basic evidence and recommend an alternative link, then. If you are so very knowledgable, you can surely do this in about 30 seconds.  Best to be positive. Montanabw 05:57, 1 November 2006 (UTC)

 * WP:CIVIL, please. riana_dzast a  02:59, 2 November 2006 (UTC)

Research issues
Noted earlier comment since removed by poster (See 'Accuracy of Article'), though it worth resurrecting for comment.

Suggest that it might be useful to explain what and how various theories are "outdated by 10 years" in the article and provide some links to current research so that those of us who care can take a look and see what kind of consensus can be reached. My point is merely that we float test balloons before diving in with wholesale edits of what clearly was an article that someone took a LOT of work to create.

I find the genetics of color quite interesting and a field that has changed beyond recognition since I took a class that discussed genetics during the 1980's. I am not surprised that even now there are still changes and debates going on...but I have also seen some head in the sand attitudes amongst people who dislike the revelations of modern genetics and attack the science itself. (Thinking here of the early days of HYPP being linked to Impressive as an example.)

I am not a geneticist, I am just a horse person with a penchant for wordsmithing and my (warning: bad pun coming) horse in this race is to try and separate what is POV from what is flat-out inaccurate (amazing how often people confuse the two). If I am convinced that something is the consensus of modern science, I am happy. If not, I like to see the various points of view presented so that people can look into the issue for themselves. (Like the eternal debate over on the wild horse article over whether equus ferus is or is not the same as equus caballus...sigh...everyone argues, no one cites to research. How can we laypeople decide if we can't review the research others have done?  Arrgh!)

Personally, I have yet to see a good research citation on the question of dominant white (WW) as a lethal, as contrasted with Lethal White Syndrome (OO). At this point, it is my understanding that both exist, but I have also seen (though am not yet convinced) some arguments that there is no such thing as the W gene at all, that all "white" horses are so-called fully-expressed Pintos...curious to hear what folks think? Montanabw 00:17, 17 September 2006 (UTC)

White Genes
Very little has actually been published on the subject of albinism in horses. One paper claims to have found the genetic marker that coincides with the White gene, but their evidence is doubtful, and the article has received no citations. http://www.blackwell-synergy.com/doi/abs/10.1111/j.1439-0388.2004.00481.x?prevSearch=allfield%3A%28white+genetic+mapping+horse%29 (Sorry: restricted access to full article.) If anything, they seem to have mistaken the sabino gene for the White gene. My discusions with experts in the field suggest few, if any, see the White gene as a plausible theory.

Current genetics tells us that horses that appear white are generally not albino, but instead contain genes for localised albinism, such as the leopard complex, the sabino complex, or various others. In these cases the white markings are fully expressed, and it is almost impossible to find any pigmented coat on the horse. This is not, however, considered true albinism, such as that supposedly caused by the White gene. Additionally, when many dilition genes are present, it is not possible to detect the presence of any pigment, and the horse appear white. This is not considered to be a form of albinism.

Currently the White theory states that the white gene is a dominant trait, so that ww codes for non-white, Ww codes for a completely white horse, and WW codes for a completely white horse with a lethal genetic illness (Lethal White Syndrome) that causes it to die soon after birth. By this theory, both parents of a LWS foal must be completely white, yet this is almost never the case. Instead, both parents have only small patches of white, caused by the Overo gene. (In very rare cases the overo gene is not present, although the horse still has the gene that codes for LWS.) Now that a genetic test exists for Overo, it has been confirmed that all LWS foals are OvOv and appear completely white, and both their parents are usually Ovov.

Since genetics tests have proven that it is not the White gene acting to cause all the traits that we have previously associated with the white gene, then this seems to be sufficient proof to say that it doesn't exist.

In case you're interested, Animal Genetics, Inc, is one of the organisations that offers genetics testing for the overo gene. You can read more about it here: http://www.animalgenetics.us/LWO.htm Bill Killed The Unicorns

 * I know UC Davis does testing also. My understanding is that lethal white syndrome is NOT in any way linked to the W gene, even if it does exist, but instead is the gene (I have seen it called both "O" and "L")(?) associated with the "frame overo" pattern (though Paint breeders have hysterics when you way this, and it IS true that LWS occurs in Tobianos and even solids, as my understanding is that it's only lethal when homozyous).  What we DO have, however, is two different lethal conditions.  One is lethal albinism where foals are usually born dead, unlike LWS foals, who are born alive, but with the genetic flaw that results in either natural death or euthanisia shortly after birth.  The "lethal albino" (for lack of a better term) is really interesting because I haven't heard it described as part of LWS, and many "white" horses out there produce offspring who are not Pintos, thus putting the "all white horses are maximally-expressed Sabino" theory to at least some question. Kind of fascinating, whatever the result. Montanabw 23:16, 11 October 2006 (UTC)

I have never come across a site, paper or expert in the field that has stated or implied that the so-called Lethal Albinism is not Lethal White Syndrome. Could you please state your sources. Thanks. Bill Killed The Unicorns 02:24, 12 October 2006 (UTC)

 * UC Davis, for one: http://www.vgl.ucdavis.edu/~lvmillon/coatcolor/coatclr3.html
 * http://www.vgl.ucdavis.edu/~lvmillon/coatcolor/fig1a.html and
 * http://www.vgl.ucdavis.edu/~lvmillon/coats.html

 * VetGen (a competitor to Animal Genetics) for another:
 * http://www.vetgen.com/equinecc.html
 * "In the presence of the dominant allele W, a horse from birth will typically lack pigment in skin and hair. The skin is pink, the eyes brown (sometimes blue), and the hair white. Sometimes such a horse is called albino. The W allele is only rarely encountered. All non-white horses are ww. The homozygous condition (WW) is lethal"

 * The piece from the Blackwell Synergy site is abstracted from a peer-reviewed journal, Journal of Animal Breeding and Genetics
 * Volume 121 Page 374 - December 2004
 * doi:10.1111/j.1439-0388.2004.00481.x
 * Volume 121 Issue 6
 * Hence, my take is that this article by Swiss researchers is every bit as good a source as anything else on Wikipedia, and from the abstract, they seem to understand that W is a "real" gene and is not the Sabino gene, though they were curious if the two were linked. As for citation, it is a 2004 piece, it takes awhile for others to jump in and write something that needs citation, especially in this field.

 * (Given that "dominant white" appears to cause prenatal death, whereas LWS foals usually die after being born, there is a significant difference there)

 * Bottom line for me is that there is no link (yet) to lethal white linked to Sabino, SB1 has been identified as a separate gene (though there may be others) and in breeds with Sabino but not the O or N Overo or LWS gene, such as Arabians, Tenessee Walkers, Clydesdales, etc., they don't have lethal white (though Arabians have a weird thing called Lavendar Foal Syndrome, which may be linked to some kind of dilution activity, as most dead foals have a diluted coat color, hence the name).
 * The theory of dominant white not existing or not being lethal in homozygous form (WW) has yet to be "disproven," and as recently as 2004 seems to be still in the mix. I would be interested in seeing sources from peer-reviewed literature that say it doesn't exist.  Hard to prove a negative, I suppose. Montanabw 23:11, 24 October 2006 (UTC)

Your sources only state that homogenous W is lethal, they do not say that the condition is different to that of Lethal White Overo. This is nothing new, and by no means implies the two conditions are sepparate.

I am yet to see anything suggesting Lethal White Syndrome is linked to Sabino. My statement was merely saying that from what I read of the article, it seemed they had mistaken the effect of the sabino gene (as far as colour is concerned) for the effect of the W gene, and it is possible they had merely mapped the sabino gene, not the W gene.

As for the article I referred to, perhaps it is a little soon to be drawing conclusions about it. Although it is unusual for an article to go this long without citations, it does not necessarily mean that this is due to poor conclusions. I therefore retract my statement suggesting as such.

And in reference to a statement you made a while ago regarding the editing of the article: "My point is merely that we float test balloons before diving in with wholesale edits of what clearly was an article that someone took a LOT of work to create." I can understand how you can feel some sort of attachment to an article you put a lot of effort into, but I do not see this as an excuse to leave inaccurate data available to the public purely for sentimental reasons. In the equine genetics inductry, new discoveries are being made all the time, so naturally, new information will have to be added to update the article, and disproven theories will have to be removed. It should also be noted that my purpose to update this article does not include revamping the entire thing, merely stating the different theories, be they true, false, or disputed, and discussing why they have such a status. You will not lose much of your work, unless it is merely repeating something that I will say in a more concise manner. I will be happy to discuss with you any ideas for improving the layout and content of this article.Bill Killed The Unicorns 13:14, 26 October 2006 (UTC)

 * I'm not a contributor on this article other than to wikify some links and tweak some grammar. I have no emotional attachment here.  My point is simply that SOMEONE went to a lot of work, and while you offer criticisms, I guess it would be more valuable if you offered more specific sources that can correct any specific errors you see in the article.  That or create a separate article or project (call it "21st century equine coat color genetics or something) where you can put in your material and then link it to this discussion page so those of us who care can maybe see it evolves into something that can be merged into the current article.
 * and
 * The W gene that can cause lethal albinism does not appear to be the same as the one mapped Sabino gene, SB1. It also isn't the same as the "O" gene (using UC Davis designation) that causes LWS.  Lethal White and Lethal albinism are two different conditions, apparently caused by separate genes.  Sabino appears to have NO connection to either condition--Sabino exists in Arabians, for example, but not the other two, and Arabians, though they have other genetic lethals like SCID, there is no documented case of any type of lethal white in Arabians.  The way I see it, the W gene has been discussed in research literature for decades and I haven't seen a source that effectively argues that it doesn't really exist...though if one exists, I'm all ears. Montanabw 05:14, 27 October 2006 (UTC)

I think you misunderstood what I said. From what I can tell, it seems the researchers have mistaken Maximum Sabino horses for Albino horses (based solely on the fact that they are all completely white). It has long been accepted that these two genes are sepparate from each other, and I don't dispute that. However, I find it interesting that in reference to the horses they studied, they state:

"It seems, that the action of the dominant white allele is not always fully penetrant, resulting occasionally in spotted look alike offspring. These horses resemble a coat colour pattern known as sabino spotting."

"All of these white born horses transmitted the white or almost white phenotype in a dominant manner to their progeny." (Note: most Maximum Sabino horses are almost completely white.)

"Among solid coat colours, dominant white (W) segregates in this light draft horse population, going back to a founder mare ('Cigale') born in 1957. According to the studbook entries, the parents of the white-born founder mare were both of solid pigmented bay coat colour, with only negligible white markings." (Note: a single sabino gene results in white markings on the face and/or legs, and could quite likely be overlooked, resulting in the horse being recorded as solid.)

"All horses were classified into two categories as either solid coloured or dominant white; the latter including also 'sabino-like spotted phenotypes'. Thus, in this study, all horses observed with the sabino-like colour pattern were treated as incomplete dominant whites." (Since the Sabino gene has already been mapped, it is clearly not Dominant White, yet in this study it seems it has been treated as such.)

"White horses carry mostly tiny residual pigmented patches and have sometimes even 'spotted', sabino look alike, offspring (Fig. 2). These 'spotted' look alike horses may again have entirely white progeny." (This is consistant with the Sabino gene inheritance.)

"Microsatellite ASB23 was not fully informative in the pedigree, as some dominant white horses (W/w) were found homozygous for one of the marker alleles." (Note: Homogenous Sabino causes Maximum Sabino.)

"In addition, a focus should be given to an accurate description of phenotype nomenclature, i.e. to the question of whether dominant white is in fact an exhaustive expression of the sabino colour pattern or the sabino phenotype the result of incomplete penetrance of dominant white?"

All of these statements can easily be explained with reference to sabino gene(s), not W. In their conclusion, the researchers all but state this (see last quote) when discussing possible future research.

Their examinations of pedigrees and offspring of the tested horses suggests evidence of Sabino patterns, but their data is mentioned vaguely, so I cannot give a definite yay or nay on this theory. The lethal nature of the genes they mapped were not studied. It was assumed all horses tested were W/w. Their evidence suggests otherwise (see the second-to-last quote), which suggests that either W/W is not lethal, or that they were not looking at W genes. Unless the horses can be shown to NOT have a non-albino condition that causes the horse to appear completely white, it cannot be concluded that the gene they mapped is actually W. You might be interested to note that the W gene the researchers refer to is consistantly given the name 'Dominant White'.

Also, I am still working on the equine genetics article I am writing. It is nothing more than a summary of all known theories in this area, so it should be appropriate for Wikipedia. It is not finished yet, because I still have to summarise the pattern genes, and the most recent discoveries and conclusions (those that have come out since I started writing it), but it should be finished soon. I will add it to the wikipedia entry once I am done, including all my sources and references. It should be noted, however, that many of them are not online. Be patient and I will get this up soon.Bill Killed The Unicorns 08:50, 27 October 2006 (UTC)

 * Cite your source, please. I'm not even sure what point you are trying to make here.Montanabw 03:24, 29 October 2006 (UTC)

Cite my sources? I already did! If you're going to respond to a comment here, please read the WHOLE thing. I don't like to repeat myself. The paper is the same one I was referring to at the beginning of this section (White genes). I even provided the link. Unfortuanately, only the abstract is available to the general public. The quotes I mentioned were taken from the body of the article. As for the point I was trying to make - I was trying to emphasize the poor quality research these people had undertaken, more specifically the number of possibly incorrect assumptions they had made, such as a horse that appeared sabino actually being albino. Bill Killed The Unicorns 05:09, 30 October 2006 (UTC)

 * As for "it seems the researchers have mistaken Maximum Sabino horses for Albino horses" I only want to note that there is NO SUCH THING as an "albino" horse, i.e. with red eyes, etc...they die in the womb, and best evidence I have is it's because of WW. I also understand LWS to be affiliated with homozygous Frame Overo gene (OO), and that "lethal albino" (WW) is NOT LWS, (OO).   I was under the impression that some people claim that there is no "W" gene at all and that all "White" horses are maximum sabinos, an assertion that I don't buy.  Not sure if that is your position.   There might be such a thing as a "Maximum Sabino," though I would like to see the evidence for that.  I suppose there could be "maximum Tobiano" horses too--after all, isn't "maximally expressed" basically the state of the horse being one big spot??
 * I sort of buy the idea that sabino is a gene-complex and may come from multiple sources...while there have been true white Tennessee Walkers, they can also produce Pinto coloring. But, I have NEVER EVER heard of a "true" white Arabian (all "white" Arabians are actually grays) nor a "true" white Clydesdale, and both carry a type of Sabino gene, but neither of which ever carry any other Pinto patterns.  My points are simple:  1)  The source-citing thing needs to be all around who are the genetics gurus you feel have superceded the work of Bowling and Spooneberg?  2)  there's no such thing as a living "real" Albino horse, no matter how you look at it,they die, and 3) If there is such a thing as a "Maximum Sabino," then there must be more than one gene responsible for Sabino coloring, because "maximum Sabino" never occurs in at leasty two breeds who have Sabino markings.  Montanabw 03:24, 29 October 2006 (UTC)

Again with the misquotes! "As for "it seems the researchers have mistaken Maximum Sabino horses for Albino horses" I only want to note that there is NO SUCH THING as an "albino" horse" What I was trying to say is that it seems the researchers see a Maximum Sabino horse, and think its an Albino horse. These researchers are not only trying to prove the albino gene exists, but also map it. You also seem to be unfamiliar with the whole White theory: WW=lethal albino, Ww=albino (carrier of lethal gene), ww=non-albino. According to Sponenberg or Bowling. By this theory an albino should be able to exist. In practice I've never seen conclusive evidence of the gene existing, but thats beside the point. Also, you keep stating that Lethal Albino and LWS are two different things, yet you never quote an expert saying as such! You might also be interested to know that not all albinos have red eyes, regardless of animal species. In many cases the eyes are blue. Other possibilities might exist. Typically, though, albinos have white hair/fur/etc, and pink skin (if applicable). A horse with the sabino gene tends to have pink skin, blue eyes (very rarely brown), and white hair on at least part of its body. So its not so unusual to think that a Maximum Sabino might be mistaken for an albino. (Technically speaking, Sabino, along with the other pattern genes, is a type of localised albinism, but not THE albinism that is supposedly caused by the W gene.)

I'm not sure where you're getting your information on sabino, but you're way out. For the sabino 1 locus, at least, one sabino gene results in sabino markings on the face, legs and occasionally belly, while two genes results in fully expressed sabino, ie: Maximum Sabino, where most or all of the horse is white. A second sabino gene is theorised to exist, but I don't know how it is supposed to act. I think the Sabino 1 gene has a genetics test for it now, so the sabino theory stated here has been conclusively proven.

As for Maximum Tobianos (ToTo?) these don't exist simply because the Tobiano gene acts in a different way to the known Sabino gene. Maximum Tovero can exist, but this is several different genes, eg: Spl, Sa, To, all acting at once to create a white or near-white horse.

I hate to say it, but your knowledge of the actions of the pattern genes seems to be pretty poor. Next time, instead of questioning my knowledge on the subject, look it up, either here or elsewhere, to find out what the generally accepted or plausible theory(s) are, THEN come discuss it with me if you feel it necessary. I'm sorry, but I really see no point in debating such easily accessible, proven information.

 * Whoa, calm down! I am far from "way off."  In fact, I am simply raising some of the same questions about your evidence, knowledge and research that you are raising about mine. (and  I really question if a group of researchers are so stupid as to confuse albinos and maximum sabinos!  I really doubt it.)  Most of what I get is from UC Davis, though I have looked at some other source material, including the frame overo "L' versus "O" gene controversy over LWS that resulted in the independent research at U Minn, and some of the stuff out of U Virginia as well.  Bowling says WW is lethal albino. (see below)
 * The SB1 gene has been mapped, and it may be maximum sabino when homozygous, but sabino coloring seems to be produced by a gene complex or by different genes--some forms of Sabino absolutely, positively cannot act like SB1 does. If Sabino coloring always produced a white horse when maximally expressed in homozygous form, then there would be true white Arabians, and I guarantee you that there is absolutely, positively no such thing as a white Arabian (all "white" Arabians are actually grays).  Some purebred Arabians carry Sabino patterning, but NEVER have pink skin (except under white markings), or blue eyes, ever.  I do not believe that there are any "white" Clyesdales, either.  UC Davis says "A mutation has recently been discovered that produces one type of sabino pattern. It has been named Sabino1 as it is not present in all sabino-patterned horses...Sabino1 is most commonly found in Tennessee Walking Horses. Other breeds in which this mutation has been found include: American Miniature Horses, American Paint Horses, Aztecas, Missouri Foxtrotters, Shetland Ponies, Spanish Mustangs and Pony of the Americas. Other breeds of horses that are known to have sabino patterns, such as Clydesdales and Arabians, have so far tested negative for the Sabino1 mutation, although the number of animals tested is low." http://www.vgl.ucdavis.edu/service/horse/coatcolor.html#sabino1

 * Here's some of my source material on albinism:
 * In horses, the white or "W" gene is known to be responsible for the absence of pigment which is usually referred to as albinism. Bowling, Ann. "Coat Color Genetics:  Positive Horse Identification."  The theory that "dominant white" is lethal in horses--when the W gene is homozygous (WW)--was first proposed as a theory in 1953 and after 15 years of test breeding, was confirmed in 1969.   Householder, D. Douglas. "The Genetics of Equine Coat Color" Texas A&M University Department of Animal Science Equine Sciences Program, publication HRG-003 (undated). The same group of researchers found that the WW gene complex was also lethal in Dexter cattle, platinum foxes, and bluefrost minks. See also  the full cite of the blackwell article is, I think:  Mau, C., Poncet, P. A., Bucher, B., Stranzinger, G. & Rieder, S. (2004) "Genetic mapping of dominant white (W), a homozygous lethal condition in the horse (Equus caballus)." Journal of Animal Breeding and Genetics 121 (6), 374-383. doi: 10.1111/ j.1439-0388.2004.00481.x. Accessed September 6, 2006 at [1]
 * So please, understand that you may not have the full picture here, either, assume good faith and realize that other people research this issue as well. I don't breed for spots, so I don't even really know why I am spending all this time arguing about it, I actually have no axe to grind other than figuring out the truth. Montanabw 05:53, 1 November 2006 (UTC)

"and I really question if a group of researchers are so stupid as to confuse albinos and maximum sabinos!  I really doubt it." Is it really that hard to imagine? Maximum sabinos and 'albinos' both have all-white hair, pale eyes, and pink skin. In the case of the former some small amounts of spotting can occur, but not always. The quotes I mentioned above have been taken from the article by these researchers, and they clearly state that any horse that appeared sabino was recorded as albino.

Evidence exists to say that there is at least two genes that cause sabino spotting (currently named sabino 1 and sabino 2). I do not dispute such a claim. I've got an email somewhere from one of the current genetics experts that goes into this in detail. I'll try to find it. Also, I might have been mistaken when I stated that homogenous sabino 1 caused maximum sabino. I was quoting from the theory that came about before knowledge of sabino 2. All that is really clear, from what I know, is that more sabino genes are needed for maximum sabino, than for 'normal' sabino. Bill Killed The Unicorns 04:06, 2 November 2006 (UTC)

 * SB1 is the gene that might be responsible for maximum sabino, according to UC Davis, from what I understand, and as I just stated above, SB1 has not ever been found in Arabians or Clydesdales, which makes sense, because they are never "white." I have seen no evidence for only two sabino genes, I think I agree that they don't know for sure all the ways Sabino occurs, but one gene so far has been mapped.
 * Here's my question about this whole thing: Are you asserting that there is no such thing as the W gene?  Are you asserting that ALL "albino" or "white" horses are maximally expressed Sabinos?  I don't want to misunderstand your position here... Montanabw 23:05, 2 November 2006 (UTC)

I'm saying there is no conclusive evidence to suggest that the White gene even exists. I don't know what causes the effect that is described as albino, but I certainly think sabino is a good possibility, although not necessarily the only one.

I know you stated earlier something about test breeding, but it should be noted that this sort of proof does not confirm the existance of White, only suggest it exists. Something similar occurred regarding Lethal Roan. Not long after the Lethal Roan theory came about, test breeding was undertaken, with the conclusion being that several healthy homogenous roans were seen. It is now thought that roan might be polygenic, in which case previous test breeding would be inconclusive, and it is now though Lethal Roan might be a possibility. Bill Killed The Unicorns 12:05, 3 November 2006 (UTC)

 * I've heard the theory that the W allele doesn't exist, but W has been discussed in peer-reviewed literature for decades, the theory is still on the UC Davis web site, and the symptoms of lethal albino sound different from Lethal White Syndrome-- and LWS is linked to Frame overo, not to sabino anyway, so I guess I would like to see whatever articles are out there saying the W allele doesn't exist...though hard to prove a negative, I suppose. I just don't buy the "all white horses are maximum Sabino" theory.  If you have some sources I can look up myself, do provide them here.  Otherwise, I am getting tired of this issue and shall await whatever appropriate edits may be made to the article. ThanksMontanabw 17:57, 3 November 2006 (UTC)

Try looking at the evidence FOR white genes. Especially some of the first evidence by (I think) Sponenberg that made him suggest the White gene in the first place. Its very shakey. (In case you can't find it, he basically states that a lot of horses appear completely white, and names the gene that causes this as dominant W -the first mention of W, I might add- then also notices that a lot of foals that are born completely white end up dying due to a colon defect, and makes the assumption that the gene that causes the foals to be white is the same one that causes the other white horses to be white. -Interpret this how you will-) The problem with many of the methods that look at the White gene is that they identify the presence of albinism solely on the colour of the horse. As i've mentioned, phenotypically, albino and maximum sabino are often identicle. According to theory they are genotypically different, but that remains to be proven. As for the differences between LWS and lethal albino, you keep stating that the symptoms are different, yet never do you state a source for it (despite my repeated requests for it), and never have I so much as heard of an expert implying this. For the last time, PLEASE STATE YOUR SOURCES!!! User:Bill Killed The Unicorns 11:46, 6 November 2006 (UTC)
 * Um, I did, above, but I'll give you a list again...the same list:
 * http://www.vgl.ucdavis.edu/~lvmillon/coatcolor/coatclr3.html
 * http://www.vgl.ucdavis.edu/~lvmillon/coatcolor/fig1a.html and
 * http://www.vgl.ucdavis.edu/~lvmillon/coats.html
 * http://www.vetgen.com/equinecc.html
 * and
 * "Coat Color Genetics: Positive Horse Identification."  The theory that "dominant white" is lethal in horses--when the W gene is homozygous (WW)--was first proposed as a theory in 1953 and after 15 years of test breeding, was confirmed in 1969.   Householder, D. Douglas. [http://animalscience.tamu.edu/ansc/publications/horsepubs/hrg003_coatcolor.pdf "The Genetics of Equine Coat Color" Texas A&M University Department of Animal Science Equine Sciences Program, publication HRG-003 (undated). The same group of researchers found that the WW gene complex was also lethal in Dexter cattle, platinum foxes, and bluefrost minks.
 * And for the last time, THERE IS NO SUCH THING AS AN ALBINO (living) HORSE. "Albino" terminology is outdated. I don't think you actually read what I wrote here. The colon defect is LWS, versus lethal albino foals who die en utero ...and Sabino appears to have NEITHER lethal albino or LWS (this is a good thing).  And, frankly, Sponenberg was far from the first to propose the W gene, and the late Ann Bowling had pretty impressive credentials and wrote a textbook on the topic, so until I hear something quite convincing, I'm sticking with them.  Now back atcha...where is your source that W doesn't exist?  List it in full here so I can look it up myself.  Montanabw 09:24, 6 November 2006 (UTC)

I DID read what you wrote. Perhaps you missed my reply. I'll state it again to save you the trouble of looking for it: those sources only state the theory of the white genes. Not once do they say the symptoms of it are different to those of LWS. In fact, they don't even detail what the symptoms are. I'm not even sure you've read your own sources. They have almost no relavance to what you are stating.

You also say that there is no such thing as an albino horse. Although this is pretty much what I've been trying to say all along, it suggests that you are not familiar with the White theory. On the same sites you list above, it says that a single (dominant) white gene results in an "albino" horse (yes, they do use that terminology), while two of them is lethal. Now lets leave the dispute about teminology out of this, and just stick to the subject of the argument.

Finally, you state that sabino has neither lethal albino or LWS. I agree with you on this point, but I think you misunderstood what I said earlier. I was trying to say that Sabino horses are sometimes identified as albino based only on their phenotype (what they look like). Other factors are not looked at to determine if they have LWS or lethal albino or nothing, so there is nothing to suggest that the horse is not albino. If other factors WERE looked at, then it would be clear whether or not the solid white horse in question was sabino or albino or something else.

As for stating my sources, if I have them on hand I do try to post a link to them. Unfortunately, a lot of my sources are not found on the internet, eg: email/verbal conversations, so backing it up with physical evidence is not always possible, unless you want names and addresses so you can research it and contact the people yourself. Some sources aren't in English either, which is clearly a problem. Another problem is the great quantity of sources. Sifting through them all to find out which ones I'm quoting is not always practical. Especially when I am quoting from a conversation - i've simply talked to too many people to know who said what. Once I post all my data on here I'll include ALL sources though, so you've welcome to sift through it all then, and critically analyse the validity of them. Bill Killed The Unicorns 12:26, 6 November 2006 (UTC)

 * "Albino," referring to a living white horse with the W gene, is an outmoded and incorrect term, whoever is using it, though I suppose it's a handy, if careless shorthand. The American Albino Registry even changed its name to reflect the reality that there are no true albinos in the horse world.  (i.e. pink eyes)  Beyond that, I shall eagerly await your results.  It will be explosive and revolutionary to have both Bowling and Sponeberg proven wrong by a lay person such as yourself. I can't wait.  Montanabw 18:33, 6 November 2006 (UTC)

Let's keep it civil shall we? There's no need for sarcasm.

My reason for stating that W does not exist comes from real sources, not things I've made up, or attempted to directly research myself. A while ago I posted on a forum the article I wrote, that I've previously mentioned. It can be found here: http://hababeri.com/erworld/index.php?topic=6002.0 This particular version of my article is incomplete and a bit old, and my knowledge of horse genetics has since improved, plus new discoveries have been made, resulting in the accuracy of some sections being a little less than perfect, but most of it should be reasonable. More importantly, it also includes all the sources I used, and a glossary of terms. Anything I have said can be backed up by the sources listed here. Some are people, not sites, so you won't necessarily be able to find them all on the internet, but you might be able to find an email address if you wish to contact them. My article does not go into a lot of detail on the White gene theories, but my sources will, if you care to look them up.

And for future reference, in animals in general, 'true albinism' does not necessarily result in pink eyes. Animals can still be correctly classed as albino without having pink/red eyes. Just google 'albinism' if you don't believe me. Bill Killed The Unicorns 03:46, 14 November 2006 (UTC)

 * I'll grant you the pink eyes issue, certainly that is true about humans. Nonetheless, UC Davis says the W gene exists.  Peer-reviewed veterinary literature confirmed its existence over 30 years ago.  Thus, I'm not making it up, either, and you assume bad faith to imply otherwise. Now, it is possible that the theory could be overturned by new evidence, and I am open to that, but as of now there is NO peer-reviewed source that disproves the theory. Certainly none in your paper--Your very concise and mostly accurate college term paper does not properly footnote any of your assertions to the source of each statement (a bibliography does not a scientific paper make) and you cite mostly material I have seen before, a lot of breed and POV websites, very few if any peer-reviewed journals, mostly secondary sources. (and FYI, they DO have a test for the Agouti gene: see http://www.vgl.ucdavis.edu/service/horse/coatcolor.html#agouti)  But if the genetics article here is inaccurate, other than this endless argument about the white gene, which I am tired of, you fail to point out any place where corrections are needed.  Let's just work on the article and give it up.  W exists for now, the notion it doesn't is an interested but unproven theory, so when the smoking gun appears in the legitimate scientific literature, we can change things later.  Montanabw 06:13, 14 November 2006 (UTC)

Upon further investigation, it seems that although the White gene has not been completely disproven, there does not exist any evidence to suggest it does exist, as confirmed by an expert I interviewed. In order for there to be a suggestion that it exists, there must be found a horse that appears to be completely white over it's entire body, and has been genetically tested and found to be negative for all known genes that could possibly cause this, including pattern genes (eg: Sabino) and dilution genes (eg: cream). As yet, no such horse has been found, and until it is, the White gene will remain an increasingly unlikely theory. Bill Killed The Unicorns 16:33, 17 April 2007

 * I cited the Mau article from 2004 and removed your comments on the main article. Per wikipedia guidelines, it is appropriate to request a source, and this one was peer-reviewed. Apparently some mainstream scientists believe the W gene does exist.  Thus, there is still sufficient evidence for it to be discussed.  "An expert you interviewed" isn't peer-reviewed research, the Mau article is.  When you have a peer-reviewed article from a legitimate published source (other than some Sabino web site) that argues that there is no W gene, then we can post that information as well and discuss the controversy. (I do think they need to clarify the lethal white language, though, it does appear to be confused with LWS. Montanabw 15:45, 17 April 2007 (UTC)

I'm afraid I don't understand your reasoning for removing the statement "Unproven Theory" from the section for the white gene. There is no genetic test for this gene, and there is debate about it's existance among prominant scientists, therefore it is a theory. Flaxen and Dominant Black are stated to be unproven theories, yet there is certainly less debate about flaxen than white. There are some conflicting views of the pangare gene, yet that is not stated to be an "Unproven Theory". The same goes for Sooty, yet once again there is no statement saying "Unproven Theory". This article seems to lack a bit of consistency. My suggestion for this article is to define what "Unproven Theory" means, and add a statement saying whether each gene is proven or not. Eg: Unproven Theory = no genetic test available, debate among scientists about it's existance. Plausible Theory = no genetic test available, no known debate among scientists about it's existance. Proven Theory = genetic test available, proven beyond all reasonable doubt. I see the pearl gene information hasn't been added in yet either. Considering how long thats been out I'm surprised. Additionally, I think there should be a bit of consistancy with the gene symbols used. I realise different scientists use different symbols, but I think we should pick one set of symbols and stick to it. Using the same symbols as those used by the UC Davis Veterinary Genetics Lab should be a start, since they do genetic testing. I'm not familiar with the symbols used in this article for the cream gene. I haven't seen any scientists using them before. I'll leave it up to you whether or not you want to add in these corrections or not. Bill Killed The Unicorns

 * By your standards, the Gray gene doesn't exist. They don't have a test for it, either.  And, if you read the Mau abstract, there does seem to be evidence for the gene, they've narrowed down the probable location of the gene.  What is not known is if it has linkage to Sabino, and sabino may be caused by a number of different genes, of which only SB1 has been mapped:  "So far, it is not known whether dominant white (W) and sabino spotting (S) share a common genetic background. In this study, a pedigree consisting of 87 horses segregating for dominant white (W) was used to genetically localize the horse (W)-locus. Microsatellite ASB23 was found linked to (W), which allowed us to map dominant white to a region on horse chromosome 3q22."  So I'd say it is overkill to call W an "unproven" theory, especially when most of the dispute isn't among experts so much as among breeders who are not geneticists.

I never said it didn't exist, just that it wasn't completely proven. And by the definitions stated above Grey would actually be classed as a plausible theory: It is generally accepted that it does exist, although a genetic test for it does not yet exist. Even if 'most' of the debate about White is among breeders, not geneticists, as you claim, there is still some debate among scientists, so therefore it is an unproven theoory. Just because you have found one group of scientists saying they think White exists doesn't mean they all think that. I have talked to at least one expert who has doubts about the white gene, even if they haven't (yet) published a paper saying as such. Bill Killed The Unicorns

 * Please note even the abstract says the W allele has been localized to horse chromosome 3q22. That's better evidence than for Gray. Now, can we just let this go? see Mau, C., Poncet, P. A., Bucher, B., Stranzinger, G. & Rieder, S. (2004) "Genetic mapping of dominant white (W), a homozygous lethal condition in the horse (Equus caballus)." Journal of Animal Breeding and Genetics 121 (6), 374-383. doi: 10.1111/

j.1439-0388.2004.00481.x. Accessed September 6, 2006 at http://www.blackwell-synergy.com/doi/abs/10.1111/j.1439-0388.2004.00481.x?journalCode=jbg —The preceding unsigned comment was added by Montanabw (talk • contribs) 01:58, 26 April 2007 (UTC).

Perhaps you should refresh your memory of the above discussion on White Genes. There is already stated more than enough evidence to show that there is debate in the scietific world about White, regardless of which side you take. I will not repeat myself. If you feel it is in the best interests of Wikipedia's readers to ignor my suggestions and remove my corrections when you have already stated you don't actually know anything about horse genetics, but are just here to edit the syntax, then so be it. I will make no further contributions to this article. It is no skin off my nose if an inaccurate article remains as is. Frankly, your over-protectiveness of an article you haven't even written, or even know anything about, is astounding. Bill Killed The Unicorns

 * I would suggest that you look in the mirror and remember the bit about people in glass houses. My passion is that wikipedia be well-written and have legitimate citations to useful mainstream research sources.  So show me your PhD. Or maybe name this famous "expert" you have talked to.  Surely that individual has peer-reviewed publication credits or an affiliation with a respected major research university?  And they must certainly know more that Dr. Mau or Dr. Bowling or Dr. Sponeberg?  I'd really like to meet this "expert"! Oh, I forgot, you're just a college kid who wrote some term paper -- and now you know even more than the published, peer-reviewed authors that I have relied upon for my edits. Ah yes, your comments and contributions are very credible. Montanabw 18:31, 27 April 2007 (UTC)

Again with the misquotes! I have never said I know more than any expert in the field, nor do I presume to think that I do. What I AM saying, is that I have not disregarded sources just because they contradict what other sources say, which is something you have clearly done with this article. This appears to be the main reason for the gross amount of inaccuracies in this article. I may not be an expert in the field, but I at least state all theories, rather than disregarding some just because I don't like them, which is more than I can say for you. You do not have the knowledge or authority to decide which theories belong in this article and which theories don't, but due to your agressiveness you are limiting what can be written here, and I feel that goes against the whole purpose of Wikipedia. Bill Killed The Unicorns

 * Cite your sources with proper footnotes in the actual article, put in verifiable material from peer reviewed sources (as I have) and I will have much less to say. Am also removing your tag on the article.  It is far more useful and constructive to use the "fact" tag on specific points with which you disagree than to slam the whole article, most of which others have edited. Oh, and please note that I have listed at least nine sources, many peer-reviewed, to support my points in this discussion.  You have cited none to support your view, the two links you provide here do not support the "all white horses are maximum sabino" theory, and the link to your term paper (that was not very well referenced anyway, I read it) is now dead.  I did correct some material in the article when you correctly pointed out the differences with the overo lethal white gene. Show me some actual university based, peer-reviewed research that disproves W, (and not just some breeder sites) that's really all I am asking here. Montanabw 23:22, 29 April 2007 (UTC)

For future reference, the "term paper" you saw was the incomplete first draft of a project I had barely started. I posted it solely to give you an idea of what sort of stuff I might be adding to the article, not to prove any particular point. Additionally, I have already stated that the White gene has not been disproven, since this would require something along the lines of genetic testing for all pattern genes, which clearly has not been achieved yet. All I've been trying to say is that it has been neither proven nor disproven, and therefore this article should state this. A quick search of Google Scholar, or any major article database, should show this.

If you insist on adding your own bias to this article, and removing any attempts to correct this, then I no longer consider this worth my time. You may have your article all to yourself. Bill Killed The Unicorns

Pearl and Silver Dapple

 * I have no problem with someone adding Pearl to the chart. If there isn't a wikipedia article on it, maybe that needs to be done too.  There is an article on Silver dapple gene, but I don't think data is in the chart yet here. I also am OK with creating some consistency with the gene symbols.  But, I  haven't the time to do it. Someone else sure can.  Best not to start a nomenclature fight, whatever is the "majority" view probably best (maybe a paragraph explaining other terminology would help.) Montanabw 16:31, 19 April 2007 (UTC)

Genetics News
Some exciting discoveries within the past month... Two new genetics test are now available. One is for the silver dapple gene, but the other is for a rare, newly discovered gene known as Pearl (aka Barlink). This gene seems to act in a very complex manner, depending on the presence of the creme gene or homogenous chestnut. I'll try to get my hands on the official article... Bill Killed The Unicorns 13:14, 26 October 2006 (UTC)

 * Interesting and way cool...what University or lab? FYI, Equus Magazine this month ran a fascinating article on Brindle coloring in horses, which is extremely rare, and may possibility be linked to chimerism, of all things--the horse literally having two sets of DNA. Very interesting. Montanabw 05:27, 27 October 2006 (UTC)

The generally accepted theory is that Brindle is as a result of chimerism. This is not a new theory, although it is possible their evidence for it might be. Still, I'd appreciate it if you could post a link for this article. It does sound fascinating. Bill Killed The Unicorns 08:55, 27 October 2006 (UTC)

 * Maybe not new in other animals, they say male tortiseshell cats are "often" chameric. But it's brand new to horses...According to the article in Equus, the Quarter Horse stallion Dunbar's Gold was the FIRST horse ever identified as a Chimera. "Horses of a Different Stripe" Equus,, Nov. 2006 p. 21.  Have print copy, not sure if they post this month's issue online yet, but it's still on the newsstands, I think.  Neither Sponenberg, who was consulted for the article, nor Cecelia Penedo, Bowling's successor at UC Davis, had ever ran into these before.  They have been under the impression that Brindle was caused by a modifier, but this is making people rethink it--maybe not all brindled horses are chimeric, but apparently it is possible that all chimeric horses are brindled.  Fascinating no matter what.  Montanabw 04:03, 29 October 2006 (UTC)

Just because the two main experts in the field have not come across this before does not mean that it is a new theory. When I was researching brindle in horses, I came across plenty of sites that stated it was chimerism, although admittedly I don't know how much proof they had for it. These people may have prooven that brindle is chimeric, but the theory for it is not recent. Off the top of my head, I can't quote any sources, but if you look it up on google, it should be fairly simple to find. Its actually quite common, as these things go. Bill Killed The Unicorns 02:13, 30 October 2006 (UTC)

 * The pearl gene info can be found at http://www.vgl.ucdavis.edu/service/horse/coatcolor.html

 * I wouldn't say "plenty" or "generally accepted theory," but I'll grant you it isn't a brand new theory--just brand new evidence.  Looks like the best set of links to older info on brindling appears to be here , but the earliest article with the chimerism theory seems to be from '99, and the evidence didn't look too strong, more an educated guess by the author.  However, what we have in the 2006 article are the first horse chimeras CONFIRMED by DNA testing.  See also   Sounds like the Quarter Horse Journal scooped Equus by about nine months.  "Extremely rare, chimmerism has been documented in other species, and is now documented in Horses as a result of the work at UC Davis. Dr. Cecilia Penedo also presented her findings at The Horse Genome Mapping Workshop that was held on Aug. 22 in Port Seguro, Brazil." Montanabw 05:49, 1 November 2006 (UTC)

Just for interest, there is a rare pattern known as white brindle. This appears to be the same as brindle, but with white stripes, rather than black. The current theory states that this is as a result of chimerism with the roan gene. Just a curiosity - i don't know how accurate this theory is, or what evidence it has. Bill Killed The Unicorns 04:06, 2 November 2006 (UTC)

End of White discussion?
The best article I have seen on the white gene issue is Overton, Rebecca. "By a Hair" Paint Horse Journal March 2004. It explains LWS and how that test works, it mentions W as a gene that really does exist and says that WW foals are actually reabsorbed as embryos, it discusses the way the LWS gene cannot be determined by coat pattern, as it can be masked by many colors, it has even cropped up in the offspring of solid-colored horses. This one may be the most useful in practical terms. Now, can we end this discussion? It's getting redundant. User:Montanabw

 * Found the site for it: http://www.painthorsejournal.com/archives/index.html The article referred to here is the 3rd one from the top. Bill Killed The Unicorns 12:29, 6 November 2006 (UTC)

Consistency within and between tables for Alleles and Formulas
There are inconsistencies in the abbreviations used. I do not know which is correct, but this is confusing to a newbie like me. I hope someone who knows what is right will get them consistent.

Formulas table uses C and CC often; I did not find a C in the Alleles table. (??C for chestnut??) Formulas also uses Ccr and CCr, which may be a combination of the unknown C and Cream. Alleles table did not seem to combine the abbreviations that way.

Alleles table mostly uses lower-case for second letter, as in Cr and Rn. However, TO is also used.

Formulas table uses RN for roan, not Rn. Uses TO for tobiano, which is consistent with Alleles table. but confusing. Signupslls 13:42, 19 October 2007 (UTC)

 * Good point, C seems to be related to the cream gene, which should be Cr, I think. Chestnut is designated by "e" (indicating lack of the "E" Extension gene which creates black coloring.)  TO, however, is correct for Tobiano, I believe.  UC Davis Veterinary Genetics lab is the leader on this stuff, I suggest that anyone who wants to work on this use their material.  Not sure how much time I will have to look into this, but I agree consistency is needed.  Montanabw (talk) 03:26, 20 October 2007 (UTC)

Updated the Cream Dilution Gene Allele table with industry standard abbreviations. If accepted, will update rest of table. —Preceding unsigned comment added by ChuckBiggs2 (talk • contribs) 02:46, 24 March 2008 (UTC)

 * Works for me. Also check in with User:Countercanter, though, she's the main genetics guru around the horse articles.    Montanabw (talk) 04:38, 26 March 2008 (UTC)

Refresher and updates
The known, not proposed, genes to date with all the mind-numbing information...(more coming, interrupted)

COAT COLOR...

Locus: Extension (E)

Gene/protein: Melanocortin-1-receptor (MC1R)

Mutation: C901T (basepair format) single nucleotide polymorphism

Notation: Wildtype = E, C901T polymorphism = e

Phenotypes

 * E/E and E/e unaffected

 * e/e loss of function of MC1R protein in the hair; aeumelanistic coat, unaffected skin and eyes

Locus: Agouti (A)

Gene/protein: Agouti Signalling Protein (ASIP)

Mutations: 11 basepair deletion in Exon 2 (Positions 2174-2184); another as yet undescribed in peer reviewed journal

Notation: Wildtype = A, ADEx2 = a; unpublished = At

Phenotypes:

 * A/A and A/a unaffected

 * a/a modified agouti signaling protein; loss of eumelanistic colorpointing in the coat, unaffected skin and eyes

Locus: Dun (D)

Gene/protein: unknown (I believe "they" know where it is...but not tellin!)

Mutations: unknown

Notation: Wildtype = D, non-dun = d

Phenotypes:

 * D/D and D/d unaffected

 * d/d unrestrained, intense pigment deposition in the coat and loss of primitive markings, unaffected skin and eyes

Locus: Cream (C) Gene/protein: Solute carrier family 45, member 2 (SLC45A2) aka Membrane associated transporter (MATP) Mutations: N153D single nucleotide polymorphism, exon 2

Notation: Wildtype = C, N153D = CCr

 * C = unaffected

 * C/CCr = hypophaeomelanism (dilute red pigment), skin and eyes superficially affected

 * CCr/CCr = hypomelanism (dilute pigment) coat, skin and eyes only faintly pigmented

Locus: Champagne (Ch)

Gene/protein: Solute Carrier 36 family A1 (SLC36A1)

Mutations: C188G single nucleotide polymorphism

Notation: Wildtype = ch, C188G = CH

Phenotypes:

 * CH/CH and CH/ch = blue eyes and pink skin at birth, changing to amber/green and mottled pink/pumpkin tones at adulthood, respectively; hypomelanism in coat

 * ch/ch unaffected

Locus: Silver (Z)

Gene/protein: Silver homolog (SILV) or Premelanosomal protein 17 (PMEL17)

Mutations: Arg618Cys single nucleotide polymorphism

Notation: Wildtype = z, Arg618Cys = Z

Phenotypes:

 * Z/Z and Z/z = hypoeumelanistic coat, unaffected skin and eyes

 * z/z = unaffected

Locus: Pearl (Prl)

Gene/protein: Unknown (no paper)

Mutations: unknown

Notation: Wildtype = prl, unknown mutation = PRL

Phenotypes:

 * PRL/PRL = hypophaeomelanism: apricot-colored coat, light tan eyes, pinkish-purple skin.

 * PRL/prl = unaffected, unless accompanied by other hypopigmentation genes

 * prl/prl = unaffected

COAT PATTERN...

Locus: Leopard (Lp)

Gene/protein: Transient receptor potential cation channel, subfamily M, member 1 (TRPM1)

Mutations: unknown

Notation: Wildtype = lp, unknown mutation/leopard complex = LP

Phenotypes:

 * LP/LP = striped hooves, mottled skin, white sclera, leopard-associated dense white regions; dense white regions may have a few small spots of pigment; predisposed to congenital stationary night blindness

 * LP/lp = striped hooves, mottled skin, white sclera, leopard-associated dense white regions; dense white regions have a multitude of large, round spots of pigment.

 * lp/lp = unaffected

Locus: Gray (G)

Gene/protein: Syntaxin 17 (STX17)

Mutations: 4.6kb duplication in intron 6; cis-acting regulatory mutation

Notation: Wildtype = g, cis-acting regulatory mutation = G

Phenotypes:

 * G/G and G/g = coat progressively loses pigment, turning gray; predisposed to melanoma and vitiligo
 * g/g = unaffected

Locus: Frame Overo (O)

Gene/protein: EDNRB

Mutation: Ile118Lys Notation: Wildtype = N, Ile118Lys = O Phenotypes:

 * O/O = ileocolonic agangliosis, 90%+ unpigmented/white, sometimes deafness, blue eyes, death within 72 hours of birth.

 * N/O = healthy; frame overo white spotting pattern, eyes often blue

 * N/N = unaffected

Locus: Sabino 1 (SB1)

Gene/protein: KIT

Mutation: KI16+1037A or r.2350_2472del or c.2350-13T>A or g.166003T>A, resulting in exon skipping

Notation: Wildtype = sb1, KI16+1037A polymorphism = SB1

Phenotypes:

 * SB1/SB1 = typically 90%+ unpigmented/white; eyes unaffected

 * SB1/sb1 = typically jagged/roan-edged markings concentrated on the head and legs and midventral line; eyes unaffected

 * sb1/sb1 = unaffected

Locus: Roan (RN)

Gene/protein: KIT

Mutation: Unknown

Notation: Wildtype = rn, unknown polymorphim = RN

Phenotypes:

 * RN/RN and RN/rn = interspersed, non-progressive white hairs except on head and legs

 * rn/rn = unaffected

Locus: Tobiano (TO)

Gene/protein: KIT

Mutation: Downstream chromosomal inversion

Notation: Wildtype = to, chromosomal inversion = TO

Phenotypes:

 * TO/TO and TO/to = unique depigmentation pattern, typically smooth, vertically-oriented, crosses the dorsal midline
 * to/to = unaffected

Locus: White 1 (W1)

Gene/protein: KIT

Mutation: c.2151C.G or g.164267C>G or p.Tyr717X, nonsense mutation from SNP in exon 15

Notation: Wildtype = W+, p.Tyr717X = W1 Phenotypes:

 * W1/W1 = presumed embryonic lethal
 * W+/W1 = lack of melanocytes in part of skin and coat; typically 90%+ white/unpigmented, with pigmented areas along the topline that lose pigmentation with age; eyes unaffected. Franches Montagnes breed.
 * W+/W+ = unaffected

Locus: White 2 (W2)

Gene/protein: KIT

Mutation: c.1960G>A or g.160670G>A or p.Gly654Arg, missense mutation from SNP in exon 17

Notation: Wildtype = W+, p.Gly654Arg = W2 Phenotypes:

 * W2/W2 = presumed embryonic lethal
 * W+/W2 = lack of melanocytes in part of skin and coat skin and coat; typically 90%+ white/unpigmented; eyes unaffected. Thoroughbred.
 * W+/W+ = unaffected

Locus: White 3 (W3)

Gene/protein: KIT

Mutation: c.706A>T or g.131675A>T or p.Lys236X, nonsense mutation from SNP in exon 4

Notation: Wildtype = W+, p.Gly654Arg = W2 Phenotypes:

 * W3/W3 = presumed embryonic lethal
 * W+/W3 = lack of melanocytes in part of skin and coat skin and coat; typically 90%+ white/unpigmented; eyes unaffected. Arabian.
 * W+/W+ = unaffected

Locus: White 4 (W4)

Gene/protein: KIT

Mutation: c.1805C>T or g.160429C>T or p.Ala602Val, missense mutation in Exon 12

Notation: Wildtype = W+, p.Ala602Val = W4 Phenotypes:

 * W4/W4 = presumed embryonic lethal
 * W+/W4 = lack of melanocytes in part of skin and coat skin and coat; typically 90%+ white/unpigmented; eyes unaffected. Camarillo White Horse.
 * W+/W+ = unaffected

Locus: White 5 (W5)

Gene/protein: KIT

Mutation: c.2193delG or g.164309delG or p.Thr732GlnfsX9, Deletion in Exon 15 produces frameshift, premature stop codon

Notation: Wildtype = W+, p.Thr732GlnfsX9 = W5 Phenotypes:

 * W5/W5 = presumed embryonic lethal
 * W+/W5 = lack of melanocytes in part of skin and coat skin and coat; typically 90%+ white/unpigmented; eyes unaffected. 6 white, 2 near-white, 4 sabino-type. Puchilingui family. 3/4 sabino-type = W+/W5
 * W+/W+ = unaffected

Locus: White 6 (W6)

Gene/protein: KIT

Mutation: c.856G>A or g.136456G>A or p.Gly286Arg, missense mutation in Exon 5

Notation: Wildtype = W+, p.Gly286Arg = W6 Phenotypes:

 * W6/W6 = presumed embryonic lethal
 * W+/W6 = 1 almost pure white Thoroughbred.
 * W+/W+ = unaffected

Locus: White 7 (W7)

Gene/protein: KIT

Mutation: c.338-1G>C or g.130210G>C or r.spl?, Splice site mutation at 3' of Intron 2, alters reading of Exon 2-21

Notation: Wildtype = W+, r.spl = W7 Phenotypes:

 * W7/W7 = presumed embryonic lethal
 * W+/W7 = solid dam and nearly all-white filly, some pigmentation around her ears, topline. Thoroughbreds.
 * W+/W+ = unaffected

Locus: White 8 (W8)

Gene/protein: KIT

Mutation: c.2222-1G>A or g.164835G>A or r.spl?, Splice site mutation at 5' of Intron 15, alters reading of exon 15-21

Notation: Wildtype = W+, r.spl = W8 Phenotypes:

 * W8/W8 = presumed embryonic lethal
 * W+/W8 = partially-white Icelandic Horse, solid-colored parents and 4 solid maternal half-siblings. Spontaneous mutation.
 * W+/W+ = unaffected

Locus: White 9 (W9)

Gene/protein: KIT

Mutation: c.1789G>A or g.160413G>A or p.Gly597Arg, missense mutation at Exon 12

Notation: Wildtype = W+, p.Gly597Arg = W9 Phenotypes:

 * W9/W9 = presumed embryonic lethal
 * W+/W9 = all-white Holsteiner, no family members
 * W+/W+ = unaffected

Locus: White 10 (W10)

Gene/protein: KIT

Mutation: c.1126_1129delGAAC or g.143284_143287delGAAC or p.Glu376PhefsX3, frameshift mutation at Exon 7

Notation: Wildtype = W+, p.Glu376PhefsX3 = W10 Phenotypes:

 * W7/W7 = presumed embryonic lethal
 * W+/W7 = 27 family members: 5 white, 5 spotted, all heterozygous. Wide range of phenotypes; apron blaze, four white legs, belly spots.
 * W+/W+ = unaffected

Locus: White 11 (W11)

Gene/protein: KIT

Mutation: c.2684+1G>A or g.169780G>A or r.spl?, Splice site mutation at 5' of intron 20

Notation: Wildtype = W+, r.spl = W11 Phenotypes:

 * W11/W11 = presumed embryonic lethal
 * W+/W11 = One all-white South German Draft Horse stallion + 3 white offspring.
 * W+/W+ = unaffected

Countercanter (talk) 00:51, 27 May 2009 (UTC)

Proposed genes
Plopping them here for now. Countercanter (talk) 02:05, 26 May 2009 (UTC)

Alternate theory: Incomplete dominant. SplSpl:classic Splash markings.Splspl:socks, face markings, may be small in the "normal" marking range or into the pinto range with or without blue eyes. splspl causes no white at all. E+E+or E+e+: Dominant black, non-fading horse. One theory, unproven and highly unlikely, is that E+ is dominant over agouti. e+e+: no effect.
 * F
 * F f
 * Flaxen: Effects visible on red or chestnut colors only.FF or Ff: Red points on ee horses.ff: Flaxen points on ee horses. Proposed theory, allele not located.
 * P
 * Pp
 * Pangare (Mealy): Lightening of hairs in limited regions. The effects of this allele appear in areas of "soft" skin, including the muzzle, behind the elbows, in the flanks, on the buttock, above or around the eyes, and along the belly.PP or Pp: Mealy or Pangare dilution of pigment.pp: no mealy looking lightening of pigment. Proposed theory, allele not yet located
 * Rb
 * Rbrb
 * Rabicano: Partial roaning with ‘coon’ tail markings. Thought to be a dominant gene by Sponenberg.RbRb or Rbrb: Rabicano markings.rbrb: No rabicano traits.
 * Spl
 * Splspl
 * Splash, Splashed White - A type of pinto horse coloring recorded in the overo family, but possibly related to other genes. Resembles reverse tobiano with white moving from the bottom of the horse towards the top. The horse's head will look as if dunked in bucket of white paint. Commonly has blue eyes. SplSpl or Splspl: Splashed markings. Splash is not associated with frame overo lethal white syndrome.splspl: No splashed markings.
 * Spl
 * Splspl
 * Splash, Splashed White - A type of pinto horse coloring recorded in the overo family, but possibly related to other genes. Resembles reverse tobiano with white moving from the bottom of the horse towards the top. The horse's head will look as if dunked in bucket of white paint. Commonly has blue eyes. SplSpl or Splspl: Splashed markings. Splash is not associated with frame overo lethal white syndrome.splspl: No splashed markings.
 * Splash, Splashed White - A type of pinto horse coloring recorded in the overo family, but possibly related to other genes. Resembles reverse tobiano with white moving from the bottom of the horse towards the top. The horse's head will look as if dunked in bucket of white paint. Commonly has blue eyes. <BR>SplSpl or Splspl: Splashed markings. Splash is not associated with frame overo lethal white syndrome.<BR>splspl: No splashed markings.
 * Sty
 * Sty sty
 * Sooty<BR>StySty or Stysty: The Sooty effect is of black hairs mixed into a body coat or any other color, may create dark bays or "brown" horses and liver chestnut. Is most visible on Buckskin or Palomino.<BR>stysty: No black mixed into coat. Proposed theory, allele not yet located.
 * E+ also noted as Ed.
 * E+ e+
 * Fading and non-fading black: proposed theory, allele yet to be located, does not appear to occur on the same locus as the E and e alleles.
 * E+ e+
 * Fading and non-fading black: proposed theory, allele yet to be located, does not appear to occur on the same locus as the E and e alleles.

Tucking in the theoretical stuff
For future reference, the diff on the theoretical colors that was tossed from the main article; http://en.wikipedia.org/w/index.php?title=Equine_coat_color_genetics&diff=292343431&oldid=286149520

I know that there is a contingent amongst the Haflinger crowd that is big on proving that there is a flaxen gene, and the Friesian folks as well as some other color breeders are bound and determined to prove there is a non-fading black. Just FYI. Montanabw (talk) 06:22, 26 May 2009 (UTC)
 * I absolutely believe that there is a gene for flaxen, and a gene for non-fading black. However, a very thorough search of the MC1R gene failed to produce ANY other notable polymorphisms, so to annotate "non-fading black" as an allele of Extension is inaccurate. Countercanter (talk) 13:06, 26 May 2009 (UTC)

And if there's going to be a table...
...let's make it a TABLE.

dun + silver + cream = Silver buckskin dun

dun + silver + 2cream = Silver perlino dun

dun + silver + prl = Silver bay dun pearl

dun + silver + 2prl = Silver bay dun double pearl

dun + cream + prl = Buckskin dun pearl

dun + 2cream + prl = Perlino dun pearl

dun + cream + 2prl = Buckskin dun double pearl

dun + 2cream + 2prl = Perlino dun double pearl

champagne + silver + cream = Amber silver cream

champagne + silver + 2cream = Silver perlino champagne

champagne + silver + prl = Amber silver pearl

champagne + silver + 2prl = Amber silver double pearl

champagne + cream + prl = Amber cream pearl

champagne + 2cream + prl = Perlino pearl champagne

champagne + cream + 2prl = Amber cream double pearl

champagne + 2cream + 2prl = Perlino double pearl champagne

silver + cream + prl = Buckskin silver pearl

silver + 2cream + prl = Perlino silver pearl

silver + cream + 2prl = Buckskin silver double pearl

silver + 2cream + 2prl = Perlino silver double pearl

dun + silver + champagne + cream = Amber silver cream dun

dun + silver + champagne + 2cream = Silver perlino dun champagne

dun + silver + champagne + pearl = Amber dun silver pearl

dun + silver + champagne + 2pearl = Amber dun silver double pearl

dun + silver + champagne + cream + pearl = Amber silver buckskin dun pearl

dun + silver + champagne + 2cream + pearl = Silver perlino dun pearl champagne

dun + silver + champagne + cream + 2pearl = Amber silver buckskin dun double pearl

dun + silver + champagne + 2cream + 2pearl = Silver perlino dun double pearl champagne

How awful, no?

There are ten options: black, chestnut, bay, dun, silver, champagne, heterozygous cream, homozygous cream, heterozygous pearl, and homozygous pearl. That is to say, the table that included all the potential coat COLORS in horses from KNOWN genes would be 10! Which, according to Google, equals 3,628,800. Since silver doesn't affect chestnut, it's rather fewer than that, but still... Countercanter (talk) 22:00, 26 May 2009 (UTC)

 * My mind just boggled!  Montanabw (talk) 00:14, 27 May 2009 (UTC)

Roan zygosity test
Surprise! Countercanter (talk) 13:57, 27 May 2009 (UTC)

 * Hm. Indirect marker test.  They like to do these.  Seems like when they do enough, they get a large enough set of samples to isolate the actual gene(s) more closely.  I know the Tobiano test started out this way, but I think they've got it more specific now.  This is also what the CA test is now, too.  Now to get the Arabian registry to quit registering Sabinos and Rabicanos as "roan."  Sigh... Montanabw (talk) 04:03, 28 May 2009 (UTC)
 * I think that indirect tests reflect the intense competitive pressure to offer a test. There are a LOT of good DNA testing services out there. But yes, I think an indirect test also helps them get a bigger sample pool. Countercanter (talk) 11:40, 28 May 2009 (UTC)

Oh my!
Okay. I can appreciate why you wrote the intro the way you did. There is a difference between "We chose this arbitrary starting point because it would be easier to synthesize this way" and "The fundamental genetic default color of all domesticated horses is "red"." In reality, the DEFAULT (that is a simple term for "wildtype") coat color is bay dun with pangare. It seems logical to me, from the presence of grullo bred-back primitive horses, that the first event that may have altered the wildtype might have been "The Breaking of Agouti." Let me rephrase. BAY is the default. Uniform black is the result of the BREAKING of Agouti. Our friends researching early domesticated horse coat colors seem to feel that "The Breaking of Extension" was one of, if not the, earliest events, too. Let me rephrase again. NON-RED is the default. Chestnut is the result of the BREAKING of Extension. I think that as the data on Dun becomes more clear, we will hear more about it, but DUN is the default state and NON-DUN is the mutation. There is precious little molecular research out there on it. Aside: The one paper I read seemed to be drawing connections between "Dun" in horses and "Dilute" in dogs, cats, and mice. Can you imagine that there is a protein whose job it is to stick to a melanin granule and drag it to a good spot in the hair? These fibers are called melanophilin, and I believe they are similar to the fibers that grab the chromosomes and drag them apart in cell division, but I am just guessing. Anyways, this review seemed to suggest that Dun and Dilute were related. I use the Horsey Genome Scan to look for the Melanophilin (MLPH) gene and it's on chromosome 6, not 8...but then I'm not sure I had an entirely good grasp of the features. It also seems like such an obvious choice, and clearly researchers have been scratching their heads over candidate genes.

The important thing I wanted to communicate is this: I think that the "base color" approach is the most digestible way to understand horse coat color genetics. However, that introduction needs to say that: we chose this method of explanation because it's easier to understand, and it has no significance beyond that. Countercanter (talk) 12:38, 28 May 2009 (UTC)

 * I get it. I think I was going on the idea of simple to complex, the "chestnut is a form of albinism" concept...not the evolutionary formula (though there is an argument for adding section on evolution of coat colors).  So to the extent I screwed up on the red/black thing, thanks for the fix, I won't argue about that one. (though I can also point to a popular horse magazine article that described it precisely that way, LOL!).  I tweaked some more, fix anything I just screwed up again!   Montanabw (talk) 01:19, 29 May 2009 (UTC)

"Dilution" heading and dun
Hmm. I understand why dun and cream are under the "dilution" heading, however, I kinda feel that dun does not belong under that heading. Dun is the wildtype, and to be categorized the same way as cream makes it look like it's a dominant mutation. Countercanter (talk) 12:41, 13 June 2009 (UTC)

 * The concept here is that I think we aren't classifying the colors based on evolutionary steps from wildtype to domestic, but rather by the phenotypical effects of progressively "switched on" genes acting in a layering fashion on the "simpler" colors, to put it in layperson's terms ... just as chestnut is a "base" coat color, though it is not a wildtype.  Genes that overlay the darker "base" colors and dilute them are dilution genes.  Dun actually IS a dominant gene... how it became un-dominant is interesting to me, just a random mutation that was a consequence of domestication??  But anyway, in terms of phenotype, we have the 2 or 3 base colors (depending on how you treat Bay/Agouti) that every single horse has no matter what, and then from there all the other genes modify those colors.  So by that standard, dun is a dilution factor.  But I also see your logic in explaining the evolutionary process.  Maybe a different section in the article describing the wildtype origins?    Montanabw (talk) 21:32, 18 June 2009 (UTC)
 * Normal extension is dominant. The faulty extension that results in chestnut is a recessive loss-of-function mutation. Normal dun is dominant. The faulty dun that results in a rich coat color is likely a loss-of-function mutation. But I gotcha. Countercanter (talk) 00:35, 19 June 2009 (UTC)

 * But the terminology "faulty" oh dear, that makes it sound like chestnuts are flawed or something! LOL! Laypeople have enough trouble with "mutation" !  (grin). We (or well, um, you, I guess)  really need to do some work on that wildtype article.  it's a confusing enough concept in these horse coat color articles, and the underlying article is pretty weak.    Montanabw (talk) 04:45, 22 June 2009 (UTC)

Wildtypes?
I saw that on some of the genes it did mention the wildtype (E+/E+ etc.) but it looks like the agouti wildtype allele is missing (A+). Is there a reason for that? Also would it be redundant to add what the wildtypes are for each gene (cream, champagne, etc)? Correct me if I'm wrong. Tiny Trot (talk) 23:56, 27 January 2013 (UTC)

 * There isn't necessarily a "wildtype" for all colors, and thus it is kind of a waste of time, as some of these are proposed or theorized (like Black, where the distinction is a supposed "fading" and "non-fading" actually...). Sponenberg's book lists some, to the extent that we can source directly to him, I'm willing to consider, but I don't want to dredge up the more dubious stuff out there.  I mean, if you want to get technical about it, variations on dun is the only actual "wild type" color of the primitive horse.   Montanabw (talk) 21:26, 28 January 2013 (UTC)

 * Alright, makes sense. Maybe in the future if there is more research done on it then we could reconsider.

 * The individual coat color articles are all way stronger than this overview, always best to pop into those before adding stuff here, no sense reinventing the wheel. Truth is, one of these days a major rehaul is what is needed here, but our lead horse genetics editor got her master's and a real job, so hasn't had time to edit for quite some time!  ;-D   Montanabw (talk) 00:36, 31 January 2013 (UTC)

Zebra striping

 * I found an image of a cross between a zebra and a pony, and it was piebald, but with the black areas zebra-patterned instead of black. Anthony Appleyard (talk) 06:35, 9 November 2015 (UTC)

 * I think I saw that image on commons too, might be good to add to Zorse.  Montanabw <sup style="color:purple;">(talk)  03:00, 12 November 2015 (UTC)

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one statement I can't find
"Horse sperm do [not] carry the color genes" and whatever follows from that, such as [the foal's color depending on the mother's genes]. It would be comparable to the human egg not carrying sex determination genes so that birth of a boy or girl depends on which human sperm fertilizes the egg. 100.15.127.199 (talk) 02:02, 17 January 2022 (UTC)

 * I'm not sure what you mean by that, but a foal's color is determined both by the sperm and the egg. For instance if an E/e mare is bred to an E/e stallion, the foal can be chestnut but only if the mare's egg passes along her e and the stallion sperm also passes along his e. If the mare's egg has E or the stallion's sperm has E, then the foal will not be chestnut. Iamnotabunny (talk) 22:09, 5 January 2023 (UTC)

title: Talk:Equine coat color genetics


text: User talk:212.247.106.130

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

title: User talk:212.247.106.130


text:
Laurelton, Queens

Laurelton is a largely middle-class neighborhood in the New York City borough of Queens and part of the former town of Jamaica. Merrick Boulevard, which bisects the community in a generally east–west direction, forms its commercial spine. It is bounded by Springfield Boulevard to the west, 121st Avenue to the north, Laurelton Parkway to the east, and Conduit Avenue to the south.

Laurelton is located in Queens Community District 13; its ZIP Codes are 11413 and 11422. It is patrolled by the New York City Police Department's 105th Precinct.

History
Laurelton derives its name from the Laurelton station on the Long Island Rail Road, which was named for the laurels that grew there over 100 years ago. It was developed by Dean Alvord and was modeled after an English village, with stately Tudor-style homes, both attached and detached. A few co-ops exist in a former garden apartment complex, there has been some new construction but no high-rise buildings, which has enabled Laurelton to keep its small-town feel.

The area of Laurelton closest to Rosedale and Cambria Heights consists primarily of single-family homes whereas the area abutting Springfield Gardens contains more multi-family homes. The area south of Merrick Boulevard contains many large, individually designed houses, while certain blocks to the north, running eastward from Francis Lewis Boulevard, have attached, Tudor-style rowhouses. Laurelton also has a series of streets with landscaped and tree-lined center malls.

Demographics
In the 1930s through the 1970s, Laurelton was home to many Jewish-American families, home to female American radio trio NBC radio vocal harmonists Three X Sisters during the 1930s, but succeeding generations since the 1960s have included various Afro-descended groups, including African-Americans, Caribbean/West Indians and West Africans, many of whom were attracted to Laurelton's more suburban-like environment.

Based on data from the 2010 United States Census, the population of Laurelton was 24,453, a decrease of 1,922 (7.3%) from the 26,375 in 2000. Covering an area of 909.17 acres, the neighborhood had a population density of 26.9 PD/acre.

The racial makeup of the neighborhood was 1.5% (366) White, 90.1% (22,032) African American, 0.3% (73) Native American, 0.7% (171) Asian, 0.5% (12) Pacific Islander, 0.4% (97) from other races, and 1.6% (391) from two or more races. Hispanic or Latino of any race were 5.5% (1,344) of the population.

Private school education

 * Cariculum Academy of Southeast Queens A Community Schoolhouse

Transportation

Belt Parkway exits 24A/B, 23A, and 22 service Laurelton. The section of the Belt Parkway known as the Laurelton Parkway was the subject of a master plan as part of the city's emerging system of greenways and bikeways. The restoration of this 1.5 mi link was completed in 2006.

The Laurelton station on the Long Island Rail Road, located at 225th Street and 141st Road, offers service via the Far Rockaway and Long Beach branches.

Residents also have access to MTA Regional Bus Operations buses, which connect to New York City Subway stops in Jamaica. The express bus to Manhattan also stops in Laurelton.

Notable residents

 * David Bergman (born 1950), gay writer/academic.
 * Joel Brind, professor of human biology and endocrinology at Baruch College.
 * Sam DeLuca (1936–2011), New York Jets right guard in the 1970s.
 * Mikey D (born 1967), rapper for Main Source and Mikey D & LA Posse.
 * David Greenglass (1922–2014), machinist and atomic spy for the Soviet Union who worked on the Manhattan Project.
 * Derrick Harmon (born 1963), NFL running back for the San Francisco 49ers from 1984-1986.
 * Ronnie Harmon (born 1964), running back, kick returner who played in the NFL for the Buffalo Bills and San Diego Chargers.
 * Marcus Jansen (born 1968), Expressionist painter. Attended PS 156 in Laurelton.
 * Hettie Jones (born 1934), poet/memoirist and former wife of writer Amiri Baraka.
 * Meir Kahane (1932–1990), founder of the Jewish Defense League.
 * Doron Lamb (born 1991), professional basketball player for Scafati Basket of the Lega Basket Serie A
 * Neil Leifer (born 1942), photographer and filmmaker known mainly for his work in the Time Inc. family of magazines.
 * Bernard Madoff (1938–2021), former NASDAQ chairman, convicted of the largest financial fraud in U.S. history.
 * Ruth Madoff (born 1941), wife of Bernie Madoff.
 * Irving Mosberg (1908–1973), politician who served in the New York Senate from 1958 to 1967.
 * Winston Rodney (born 1945), reggae music legend, known as "Burning Spear".
 * Elliot Sperling (1951–2017), expert on Tibetan history and the Tibet-China conflict and chair of Central Eurasian Studies at Indiana University

title: Laurelton, Queens


text:
Mine Yoshizaki

Mine Yoshizaki (吉崎 観音) is a Japanese manga creator. His most well known works are Sgt. Frog, a manga he created which later received an anime adaption, and Kemono Friends, a multimedia franchise for which Yoshizaki serves as concept designer.

Career
Yoshizaki was born in Isahaya, Nagasaki. As a graduate student of Nagasaki University, he started from drawing his own dōjinshi, based on video games that were famous at that time (somewhere in the 1980s). With that dōjinshi, he practiced and improved his drawing skills day by day. Yoshizaki said that his experience in drawing dōjinshi was the most priceless experience that he ever had. According to him, making dōjinshi gave him the opportunity to seek through the world of the manga industry, with all aspects from drawing to producing (meeting with printers, editing process etc.). This allows him to do all the work, rather working in a big-scale production company that lets him work in one particular branch.

Yoshizaki later worked as an assistant to manga artist Katsu Aki. His first publication was featured in a compilation book published by Shogakukan in 1989.

He is best known for his manga Keroro Gunso, published as Sgt. Frog in the United States, which was first published in the Japanese manga magazine Shōnen Ace. He is also the creator of Arcade Gamer Fubuki and did character designs on the series Seven of Seven. In 2005, Sgt. Frog received the 50th Shogakukan Manga Award for children's manga.

Due to various Gundam references, an ongoing Sgt. Frog anime was produced by Sunrise, the original creators of the Gundam franchise. The show’s main sponsor is Bandai, Sunrise’s parent company, and the maker of the plastic model Gundam kits commonly seen in both the manga and anime (also known as "Gunpla" in Japan). This led to Yoshizaki collaborating on certain Gundam projects, such as designing the mascot girls Reiko Holinger and Catharine Blitzen for the Gundam Card Builder game.

He was also the designer of the Angel-XX figurine series from Neon Genesis Evangelion.

He provided character designs for the 1999 PlayStation video game Pop'n Tanks.

He later was a character designer for the Konami Gradius-type shooter Otomedius. This is significant because, instead of simply moving a fighter craft around, the player controls a unique character bound within a vehicle.

He has also designed a playable character called Angol Fear (a nod to his character Angol Mois in Sgt. Frog – they even wield similar weapons) to the fighting game Soulcalibur IV. He also is credited as concept designer for the Kemono Friends franchise, including the anime series.

Works

 * 1993–1995: FANTASWEAT
 * 1993–1995: Detana!! TwinBee (spin-off from the video game series Twin Bee)
 * 1994–1995: 8BIT FIGHTER SHIEN
 * 1995–1997: Space Juubei
 * 1996–1998: VS Knight Lamune & 40 Fire (tie-in manga)
 * 1998–2002: Arcade Gamer Fubuki
 * 1999–present: Sgt. Frog (story and design)
 * 1999: Pop'n Tanks (character design)
 * 2000–2003: Dragon Quest Monsters +
 * 2005: Taisen Hot Gimmick: Axes-Jong (partial character design)
 * 2007–2011: Otomedius (spin-off from the Gradius series)
 * 2015: Kemono Friends (concept design)

title: Mine Yoshizaki


text:
Talk:Color circle

Re:Merger
I don't think that a merger is a good idea. Color theory relates to the applications of color mixing in art - the Color circle relates only to the psychophysics of color - i.e., it relates to psychological laws rather than to aesthetic theory. As such, it would be like merging an article on acoustics with one on music. Grutness...  wha?  06:58, 1 Jun 2005 (UTC)

About merger
The article certainly needs to be expanded to make it more informative and the image should be 'better'. I am in favor of the proposal that this article be merged with color theory and a special mention be given of the psychological part of it.
 * If it's to be merged anywhere, it should be with color vision, not color theory. It has a everything to do with color vision, and nothing whatsoever to do with color theory. I hate to resort to the clichéd "I know what I'm doing" line, but as a former researcher in visual perception who now works as an artist and arts reviewer, I do know what i'm talking about here... Grutness...  wha?  14:24, 20 Jun 2005 (UTC)

questions and answers
''what's a "luminance complement"? when mixed how in the correct proportions?''
 * Answer: A luminance complement is one used with additive - that is, emanative, colour, as opposed to the mormally accepted subtractive meaning of the term, as used with paint. As to which correct proportions, that all depends on the two lights being mixed. Generally, however, when a light of sufficient brightness is added to its luminance complement, a neutral grey or white will be produced. This is not true when two lights which are not luminance complements are mixed, irrespective of the brightness of the two lights

I'm not sure that subtractive color is inherent to the concept of a color wheel.
 * That's not the point - that it is primarily used with subtractive colour (and every colour wheel I've ever heard described deals with pigment, and is thus inherently subtractive) does not rule out the possibility of it being used with additive colour. The colour circle is NEVER EVER used with subtractive colour

''this rather depends on the specifics of the color wheel being used, doesn't it? A munsell hue wheel is going to look different than an RYB one.''
 * Answer: Well, that's exactly my point. There is a specific colour circle, but there is not a specific colour wheel. A Munsell hue wheel, a Winsor and Newton oil colour wheel, a Faber aquarelle wheel, an individual artist's wheel - all will be different. A colour circle is the colour circle of normal human vision and has no variant forms.

--questions by jacobolus. answers by Grutness —Preceding unsigned comment added by Jacobolus (talk • contribs) 07:55, 20 September 2007 (UTC)

 * Is there an explanation for how the colors were spaced around the color circle? Even assuming you leave additive complements (with some particular target white point) directly across from each-other on the circle, that still doesn't decide how much of the wheel to devote to each part of the spectrum.  Is this just scrunching u*v* chromaticities into a circular shape, or what?  --jacobolus (t) 08:02, 20 September 2007 (UTC)
 * Good question, and I'll admit I've no idea. It isn't mentioned in any of the texts I've got here either. I'll have a look in the university library next week and try to get an answer. Grutness...wha?  08:12, 20 September 2007 (UTC)

Interesting ideas. I've been in color science for a while, and what you're referring to as a luminance complement was always just called a complement, or an additive complement. I don't find "luminance complement" in a single book in Google Book Search; see this book for additive complement. Where does luminance complement come from? Gregory? Dicklyon 14:36, 20 September 2007 (UTC)
 * mmmm. Good question. I can't find it with that name in any of the texts I mentioned (though it is written as that in my old psych notes, I see). Additive complement is probably a better name, in that case. Grutness...wha?  23:11, 20 September 2007 (UTC)

title: Talk:Color circle


text: User talk:69.231.117.173

title: User talk:69.231.117.173


text:
Cherry Heering

Heering Cherry Liqueur is a Danish liqueur flavored with cherries. It is often referred to simply as Peter Heering or Cherry Heering in cocktail recipes. Heering Cherry Liqueur has been produced since 1818, and the company is purveyor to the Royal Danish Court and formerly to Queen Elizabeth II. It is sold in more than 100 countries.

Heering Cherry Liqueur is an ingredient of cocktails including the Singapore Sling and Blood & Sand. Cherry Heering is used in baking; some of the alcohol evaporates as part of the process.

Historically produced by the Peter F. Heering company in Denmark, the liqueur brand was acquired by Dutch spirits group DeKuyper for an undisclosed sum in October 2017.

title: Cherry Heering


text:
Heino Eller Tartu Music College

The Heino Eller Tartu Music College is a music school in Tartu, Estonia, founded in 1919. It received its current name in 1971, after the Estonian composer and music teacher Heino Eller, who taught at the school from 1920 until 1940.

Tartu School of Composition
Heino Eller's return to Tartu in 1920, to teach in the Tartu Music School, led to the development in the 1920s–1930s of the Tartu school of composition

In the 1920s, the school was named Tartu Higher Music School (Tartu Kõrgem Muusikakool).

Those identified with the school include:
 * Composers
 * Heino Eller (originator)
 * Eduard Tubin
 * Eduard Oja
 * Olav Roots
 * Alfred Karindi
 * Johannes Bleive
 * Music theorists
 * Karl Leichter
 * Faculty
 * Salme Kann
 * Harald Laksberg

title: Heino Eller Tartu Music College