genetics of black bay

[motorgypsy]

I was looking at the photo posted in the sales section and wondering if anyone had done the agouti test on a black bay. Is the coloring due to the soot/smut gene or are they true blacks with the mealy/pangare gene?

http://i270.photobucket.com/albums/jj98/Nougatnator/malattia0508_2.jpg

This great photo is posted in the sales section and is a really good example of black bay. You will notice the horse looks totally black except for the muzzle and a slight lightening at the flank.

http://img.photobucket.com/albums/v99/motorgypsy/IM000302a.jpg

another black bay.

Anyone??

[paintedhorizon]

Can't sooty cause the brown on the muzzle?

[motorgypsy]

Sooty darkens the body - usually top part more than the belly but it won't turn the face lighter than it already is. Sooty is usually kind of uneven so the horse has different color intensities at different part of the body. It's possible that if a horse is homozygous for the sooty gene and is bay that the gene may double in effect like the creme gen does. Sooty turns red chestnuts to liver chestnuts and buckskins to sooty buckskins that have a lot of black on top of the creme body. And it will give you darker palominos also. Pangare or the mealy gene is the one you see a lot draft horses with it but it's in paso finos also. It lightens the muzzle and flanks turning them almost creme in a red bay so IF it acted on black as well as bay it could turn a genetically black horse into what looks like a black bay or a black horse with lighter muzzle, flanks etc. But we haven't had our two black bays tested for the A agouti gene that produces bay from black so we don't know if they have it or not.

I know there is speculation that there is a brown color but I haven't seen documentation of it anywhere.

[SandyMM]

UC-Davis says call it what you want - it's still a bay.....

[paintedhorizon]

I disagree Sandy, that mare up top is a dark brown, not a bay.

[SandyMM]

UC-Davis says bays are bays.... If it has black points and no dilutes, it's a bay.

[Mellifluous]

A bay is a bay is a bay. There are many different shades and sooty can really darken a bay. Phoebe is a great example of a bay with the sooty gene. She gets a little bit darker every year.

There are also fading blacks which sometimes are mistaken for dark bays. They are different from non-fading blacks.

[PasoVicki]

Until (1) there are tests for every equine color factor, and (2) the horses in question have been tested -- there's no way to know for certain. So there will always be conflicting opinions.

[cristy]

I have always heard a horse of that color called a seal bay. Black with brown muzzle and flanks.

[paintedhorizon]

Okay, so what's a brown then?

[SandyMM]

Per UC-Davis:
The alternative allele a does not restrict the distribution of black hair and thus in the presence of the allele E of the E gene a uniformly black (Fig. 1H) horse is produced. In most breeds of horses, the a allele is rare, so black horses are infrequently seen. Many black horses will sun-fade, especially around the muzzle and flanks and such animals may be called brown. The term brown can be used for several genetic combinations (various reds, bays and dark bays (Fig. 1I), as well as some blacks).
A bay may be _called_ a number of things depending on the shade of bay, but they're still genetically bays. A black, bay, or chestnut may be called 'brown', but they are still genetically black, bay, or chestnut.

[PasoVicki]

I read about a genetic study . . . from France, I believe . . . which found the color brown was caused by a variation of the agouti gene. The researchers found two distinct agouti genes, one of which caused bay and one of which caused brown.

[paintedhorizon]

Brown is homozygous or heterozygous extension (EE or Ee) and agouti (AA or Aa), heterozygous for pangere (Pp) and homozygous sooty (StySty)
E? A? Pp StySty

Seal Brown is homozygous or heterozygous extension (EE or Ee) and agouti (AA or Aa), homozygous for pangere (PP) and homozygous sooty (StySty)
E? A? PP StySty

Dark Bay is homozygous or heterozygous extension (EE or Ee) and agouti (AA or Aa), and homozygous sooty (StySty) no pangere
E? A? pp StySty

Golden Bay is homozygous or heterozygous extension (EE or Ee) and agouti (AA or Aa), and homozygous pangere (PP) no sooty
E? A? PP stysty

Mahogany Bay is homozygous or heterozygous extension (EE or Ee) and agouti (AA or Aa), can have any form of pangere (PP, Pp, pp), and heterozygous sooty (Stysty)
E? A? ?? Stysty

Red Bay is simply homozygous or heterozygous extension (EE or Ee) and agouti (AA or Aa), no pangere or sooty
E? A? pp stysty

And lastly, Wild Bay is homozygous or heterozygous extension (EE or Ee) and agouti (AA or Aa), and homozygous or heterozygous pangere (PP or Pp) no sooty
E? A? P? stysty

So no, genetically, there are differences between bays and browns.

[SandyMM]

Information source?

[PasoVicki]

Brown is homozygous or heterozygous extension (EE or Ee) and agouti (AA or Aa), heterozygous for pangere (Pp) and homozygous sooty (StySty)
E? A? Pp StySty

Seal Brown is homozygous or heterozygous extension (EE or Ee) and agouti (AA or Aa), homozygous for pangere (PP) and homozygous sooty (StySty)
E? A? PP StySty

Dark Bay is homozygous or heterozygous extension (EE or Ee) and agouti (AA or Aa), and homozygous sooty (StySty) no pangere
E? A? pp StySty

Golden Bay is homozygous or heterozygous extension (EE or Ee) and agouti (AA or Aa), and homozygous pangere (PP) no sooty
E? A? PP stysty

Mahogany Bay is homozygous or heterozygous extension (EE or Ee) and agouti (AA or Aa), can have any form of pangere (PP, Pp, pp), and heterozygous sooty (Stysty)
E? A? ?? Stysty

Red Bay is simply homozygous or heterozygous extension (EE or Ee) and agouti (AA or Aa), no pangere or sooty
E? A? pp stysty

And lastly, Wild Bay is homozygous or heterozygous extension (EE or Ee) and agouti (AA or Aa), and homozygous or heterozygous pangere (PP or Pp) no sooty
E? A? P? stysty

So no, genetically, there are differences between bays and browns.

Are there genetic tests now for pangere and sooty?

[SandyMM]

UC-Davis Color (http://www.vgl.ucdavis.edu/services/coatcolor.php#assign)

[Mellifluous]

I think it is great that we can have such in depth questions and conversation on one of the most under rated colors in the equine realm. After all, haven't you been told it is just a plain ole bay horse. :p

[CarolU]

Okay, so what's a brown then?

I was always taught that brown was one of the primary horse colors (bay, black, white, gray, brown, sorel/chestnut). I swear the only brown horses I've ever seen were liver chestnuts.

Diablo is registered as brown. He, Bien and Buddy are all the same color, seal bay. Bien and Buddy are registered as bays.

[SandyMM]

Emi's dam, Candida Real, was registered as a brown. She looked like a drk chestnut in the only picture I ever saw. Maybe somebody who knew her could describe her color.

Emi is a dark bay who has 20 offspring (4 not yet listed on pasoregistry:
75% were Bay (http://pasoregistry.com/db/Children.asp?ID=82254&Color=Bay)
6% were Buckskin (http://pasoregistry.com/db/Children.asp?ID=82254&Color=Buckskin)
->6% were Chestnut (http://pasoregistry.com/db/Children.asp?ID=82254&Color=Chestnut)
6% were Dark Bay (http://pasoregistry.com/db/Children.asp?ID=82254&Color=Dark%20Bay)
6% were Gray (http://pasoregistry.com/db/Children.asp?ID=82254&Color=Gray)
6% were Pinto (http://pasoregistry.com/db/Children.asp?ID=82254&Color=Pinto)

His sire, Coral, was a bay with a red gene as evidenced by a number of chestnut offspring.
52% were Bay (http://pasoregistry.com/db/Children.asp?ID=70258&Color=Bay)
1% were Brown (http://pasoregistry.com/db/Children.asp?ID=70258&Color=Brown)
12% were Buckskin (http://pasoregistry.com/db/Children.asp?ID=70258&Color=Buckskin)
22% were Chestnut (http://pasoregistry.com/db/Children.asp?ID=70258&Color=Chestnut)
3% were Gray (http://pasoregistry.com/db/Children.asp?ID=70258&Color=Gray)
10% were Palomino (http://pasoregistry.com/db/Children.asp?ID=70258&Color=Palomino)
1% were Roan (http://pasoregistry.com/db/Children.asp?ID=70258&Color=Roan)

His dam, Candida Real, was registered as brown and never produced a single chestnut even when bred to a chestnut (Cantante de Omega) - the offspring was _bay_!
30% were Bay (http://pasoregistry.com/db/Children.asp?ID=70392&Color=Bay)
10% were Black (http://pasoregistry.com/db/Children.asp?ID=70392&Color=Black)
25% were Buckskin (http://pasoregistry.com/db/Children.asp?ID=70392&Color=Buckskin)
15% were Gray (http://pasoregistry.com/db/Children.asp?ID=70392&Color=Gray)
20% were Pinto (http://pasoregistry.com/db/Children.asp?ID=70392&Color=Pinto)

What do you want to bet Emi's single 'chestnut' offspring is actually 'brown'???
Eminente de MiLE (dark bay from bay/red and brown) x Elysia de Vez (black from two black parents)= Federal Expreso de CB (http://pasoregistry.com/db/Tree.asp?ID=88072)

Curioser and curioser!

[cristy]

I've never seen a horse that I would call brown. tree bark is brown. horses are chestnut or bay or sorrel or dun and all the variations of these colors.

[Siggy]

I dont know a lot about genetics, but a friend of mine emailed me this information because I posed the brown question to her

The Agouti gene is responsible for one of the most common horse colorations, the bay. It's a modifier gene which restricts black eumelanin pigment to a horse's lower legs, mane, and tail. This means that while a chestnut horse can carry the dominant Agouti gene, the bay coloration will only be visible on a black horse. Afterall, the Agouti gene can't restrict a chestnut's black pigment, because a chestnut has no black pigment!

Different than most genes, the Agouti has more than two possible alleles. It has a total of four! Of course, this would mean that there can't be a simple dominant and recessive relationship. Instead, there's an order of dominance with each allele having its place. You can see this for yourself by cycling through the Agouti alleles below.

The most recessive allele, denoted as "a," does nothing and is therefore the only one that allows a horse to remain its original black. Being the most recessive among four different alleles, however, means it is easily overwritten. This is part of the reason that black horses are so uncommon.

One step up from this is is the allele denoted as "At." It restricts black pigment from the soft areas of a horse's body, resulting in the coloration known as seal brown.

Next is the most commonly found allele, and the one which was first discovered. It's simply denoted as "A," and causes the normal bay coloration. A regular bay will have black on its legs extending up to or above its knees. Its mane and tail will be black, and it may even have black tips on its ears.

Finally, the most dominant of all the Agouti alleles is the "A+" allele. It creates a wild type bay which will have a black mane and tail like a regular bay. However, the black on its legs only extends as high as the pastern (ankle) and often the horse's red color is somewhat lighter.

[motorgypsy]

sources please.

I had read about the wild bay but I read recently that while the phenotype described as "wild bay" does exist that it does not for example dilute dun markings and has not been identified.

The information about golden bay is very interesting because we have a "golden bay" phenotype in Adriel, Arwen's younger sister and it says golden bays have the pangare gene. Well I don't know where our's would have gotten it with a really intense blood red bay with no pangare mother and a grulla Ee aa father who shows no pangare either.

So I guess my question is will EE plus pangare produce what is called a black bay. For a horse to be REALLY a bay it must have at least one A. But I wonder if there are any genes like pangare that lighten the face and flanks that can make a black look black bay.

By the way Michelle, the horse Stella is riding may be dark brown but that could be from sun bleaching. Homozygous true black will bleach very brown because we board with one. The difference was amazing when they let him run during the day and when he was out all nioght and in during the the day. he is a true black TW but he is brown when he stays out in the summer sun even with some shade.

But Arwen, in the second picture was as black as coal as the old saying goes except for the tiny tinge of brown on her muzzle. She is a true black bay. We need to get her tested for A now that my curiosity is up on it.

We have a second black bay and we didn't realize just how black she was until we put a white fly sheet on her one summer. Again just the brown on the muzzle was all she showed with a jet black body.

Here is where she is bleached out
http://img.photobucket.com/albums/v99/motorgypsy/IM000140.jpg

and here she was nearly black but I didn't get a photo of her when she was really really black. Her father was a black bay or dark bay by the way but he looks almost black in his photos. I thought he was black but his owner said no, he was dark bay.

http://img.photobucket.com/albums/v99/motorgypsy/kahluashowsmall.jpg

Regarding brown, in PFHA a black bay is registered as a brown. Arwen is registered as a brown. The description was black body with brown muzzle and maybe flanks if I remember correctly. But whether there is actually a gene that will turn black into brown other than the silver gene which does appear to do that, - I haven't seen definitive evidence of at any of my sources.

Regarding fading blacks the latest I've read on this is that genetically black is black and heterozygous and homozygous blacks are the same color and behave the same way - and they'll all bleach in the right conditions - rain plus a lot of sun plus high humidity equals hydrogen peroxide which bleaches any color hair. I know morgans register fading blacks but i haven't seen any genetic difference and have read that there isn't any.

One other thing that can change black slightly is the creme gene. On some blacks it's not noticeable but on others it can give them a strange color. This combination of EE or Ee plus one Cr may be the genetic makeup of what people call fading blacks. I really don't know on that one.

[cristy]

Diego is seal bay and he is registered just as bay. His description says nothing special.
http://i139.photobucket.com/albums/q310/cristy5513/sendablecompy.jpg
Tante is registered a bay and under description it says dark bay.
http://i139.photobucket.com/albums/q310/cristy5513/7_8_20041_54PM_0005.jpg
Volante is registered a bay and under description it says seal bay.
http://i139.photobucket.com/albums/q310/cristy5513/zonapics321.jpg
It all depends on what you write on the paper that you send what PFHA calls it. These horses were registered by 3 different people but they are all the same color. Obviously if you send pics of a chestnut horse and say it is bay that will not fly but PFHA tends to go with whatever language is used on the papers if it is accureate.

[Mellifluous]

When agouti was sequenced, they found two alleles 'AA' and 'Aa'. There is no color correlation with homozygous/heterozygous. Currently, there is no genetic difference between a wild bay, a normal bay, etc. Agouti is not the gene that is responsible for the variations and the culprit has yet to be found. 'At' and 'A+' are old and now disproven theories.

In fact, pangare and sooty are actually refer to theories and not identified genes. Part of the issue with color genetics is that so many theories are presented as fact. I am trying to learn all that I can and have my a lot of ideas about things that I am waiting for tests on to see if they are true.

Oh, and Cr does not have anything to do with fading blacks. Fading blacks are still genetically black, a black with cream is something totally different, typically referred to as a Smokey black with one cream gene or a smokey cream with 2 cream genes.

[Siggy]

this is so interesting, where did you find that the 'At' and 'A+' is old information? how do you find the most current information, I would love to have more information on my "brown" colored horse (not a PF).

[paintedhorizon]

My source is a college student that is studying to be a vet and her major is equine genetics. She got it from her professor. Ask me a color and I can pretty much tell you the genetics.

As far as dark brown versus dark bay, they are completely different to me. Embellazo is a dark brown, he is NOT a bay. He throws mostly dark browns and blacks, with an occassional chestnut thrown in the mix.

[Siggy]

so what is the genetic markers of an actual brown horse?

[Mellifluous]

I don't think there is one for a brown horse yet.

The really confusing thing about color genetics is that there is always new information coming out, some of it fact and some speculation! There are respected folks out there with books that contain both fact and theory and it is difficult to seperate the two with the way that they are written. Add on top of that that some college professors and "color" breeders are operating on dated or incorrect information and it gets even more confusing.

[Siggy]

yes - that is how science works, theories then proving or disproving. Can you tell me where the information that you mentioned was disproved - I have found a number of things mentioning that brown is a color - then the agouti info that I posted - you say was disproved lol, so I need to move on the next ones I have found but would like to know how/when that info was found to be incorrect. round and round we go again

[paintedhorizon]

Per the college professor at her college, this is brown.

Brown is homozygous or heterozygous extension (EE or Ee) and agouti (AA or Aa), heterozygous for pangere (Pp) and homozygous sooty (StySty), no creme (cc), dun (dd), champagne(chch), gray(gg), roan(rr) or silver(zz), flaxen doesn't affect it either way, so the horse could carry flaxen and not show it (??)
E? A? Pp StySty cc dd rr zz gg chch ??

[PasoVicki]

My source is a college student that is studying to be a vet and her major is equine genetics. She got it from her professor. Ask me a color and I can pretty much tell you the genetics.

But this student is giving you theories, not tested and proven facts -- correct? As Mel said, there are lots of theories floating around, but until those theories are proven to be true (or false), they shouldn't be stated as facts. Doing so only causes confusion. And there's already plenty of confusion. :)

[SandyMM]

You guys are worried about brown and our association still lists _albino_ as a color and lists 27 horses as albino..... the first one on the list is from a dun and a buckskin....

[Siggy]

I could not find a lab that was able to test for pangere or sooty so not sure that those are actual markers or currently theories. I did find a lab that mentions the seal brown test is coming soon so I will be contacting them for sure and ask if they have any info on the internet about it.

[Siggy]

You guys are worried about brown and our association still lists _albino_ as a color and lists 27 horses as albino..... the first one on the list is from a dun and a buckskin....


The association is not a lab and have not updated their information in decades. We are dealing with current information and how actual genetic markers are being found. Everyone pretty much knows now that there is no albino horse (except PFHA that is)

[Mellifluous]

pangere and sooty are not mapped yet so are currently in the theoretical realm.

It is that way with many of the things we see, like dun. We all knew it was there but weren't able to ID it genetically until recently. It was just a few months ago that the zygosity test was released for Dun.

PFHA needs to get their stuff together when it comes to color. It would be really really nice to know things like the base color of greys!

[SandyMM]

It would be really really nice to know things like the base color of greys!
Now _that_ would be useful!

Emelina who is Eminente de MiLE (dark bay) x Katia Linda de las Viejas (chestnut) is so dark we really haven't made a definite decision as to her color.... She is one that will need a color test done to identify black or dark bay.

[motorgypsy]

Diego LOOKS what I call sooty. Irregular black patterns particularly on the back but extending down the sides. You notice that the second horse doesn't look like that and neither does Arwen and she never has. When Kalua turns brown it is even, not like the sooty horse looks.

As a career educator, perpetual university student and assigner and evaluator of science research I can tell you that what Mel says is very correct. For example Dr. Sponenbburg sp? is widely regarded as a pioneer in the field of equine genetics but his book came out in '04. Since the horse genome project started bringing in results a great deal of his information was verified and much of it was NOT verified.

When I used to assign research I had two criteria for sources the students could use as background information on their topic - experts in the field who were currently doing research on the topic and the first line science journals. All other sources were secondary and therefore very likely not valid or perhaps partially valid but just not first line information.

IF the student's professor you mentioned Michelle actually WORKS/ED on the genome project and published about the results he/she would be a first line source. If not - he/she is only a second line source whose information would be superceded by all first line sources.

In my first college physics course my professor told us "the first thing my physics professor told us was 'the ATOM CANNOT BE SPLIT'" He said the headlines of the newspaper the next day read THE ATOM IS SPLIT. That's science. It changes from day to day and hour to hour.


Here is a link about the genome project. It says they have completed the first draft of a horse has been recorded.

http://www.uky.edu/Ag/Horsemap/

and here is the list of people in the US working on this project

http://www.uky.edu/Ag/Horsemap/northamerica.html

[Mellifluous]

This is a good way to think about color.

Is it testable and verifiable? yes - good, then you can talk about it as fact. no - then make sure you are being clear it is a theory, in many cases a plausible theory but still theory.

[paintedhorizon]

I will let you know as soon as I hear back from her.

[paintedhorizon]

Per UC Davis

The basic coat colors of chestnut, bay, brown and black horses are controlled by the interaction between two genes: Extension (gene symbol E) and Agouti (gene symbol A). The Extension gene (red factor) controls the production of red and black pigment. Agouti controls the distribution of black pigment either to a points pattern (mane, tail, lower legs, ear rims) or uniformly over the body. The effects of approximately 10 other genes may modify these pigments to provide an array of colors in the domestic horse ranging from white to black.


Currently, genetic tests are available for: Extension (Red Factor), Agouti, Cream Dilution and Lethal White Overo.

The gene that controls the distribution pattern of black hair is known as A. The allele A in combination with E will confine the black hair to the points to produce a bay (Fig. 1G). Various shades of bay from brown, dark bay through mahogany bay, blood bay to copper bay and light bay exist. The genetics of these variations has not been defined. Any bay horse will include A and E in its genetic formula as well as ww and gg.

Black pigmented horses (black, bay, brown, buckskin and grullo, to name a few) have at least one E allele.

Red Factor results are reported as E/e Both black and red factors detected. The horse can be assumed to be heterozygous for the red factor (Ee). It can transmit either E or e to its offspring. The basic color of the horse will be black, bay or brown, but depending on genes at other color loci, the horse may be buckskin, zebra dun, grullo, perlino, gray, white or any of these colors with the white hair patterns tobiano, overo, roan or appaloosa.

[motorgypsy]

Good point - please do give sources for your information. And tell us if the gene/s is proposed or verified.

This came from horsecolor.com BUT although it says the brown gene has a test it doesn't say who does it.

Brown (AtAt or Ata, plus EE or Ee)

http://www.horsecolor.com/images/brown_sm.jpg (http://www.horsecolor.com/images/brown.jpg)There is now a DNA test to differentiate this color from bay or black. It's definitely a separate and distinct color meriting a category of its own. The color is called "black and tan" in some countries, which is an apt description. The basic appearance is that of a black horse with tan highlights in specific areas -- the muzzle, flanks, underbelly, and girth areas. The darkest shades of seal brown would be almost all black except for a little tan at the muzzle and flank, while the lighter ones look more like a tan horse with an overlay of black covering a good deal of the body, and the very lightest shades of seal brown might look very much like some bays. At one time a theory was proposed that seal brown was caused by a solid black base color with a 'pangare' gene, however, this theory was disproved when the a allele was isolated and a test for it developed -- since none of the seal browns that have been tested turned out to be aa, they could not be "black plus" anything.


It also doesn't give a source for this information.

[PasoVicki]

Various shades of bay from brown, dark bay through mahogany bay, blood bay to copper bay and light bay exist. The genetics of these variations has not been defined.

Even UC Davis is admitting (although in a 'round about' way) that their theory about brown is only a theory -- not proven as fact. It could very well turn out that they are totally wrong, and brown is caused by some unknown genetic factor.

[paintedhorizon]

However, UC Davis says elsewhere on their site that brown is a basic coat color. And they also list it separately instead of with bay elsewhere.Per UC Davis

The basic coat colors of chestnut, bay, brown and black horses are controlled by the interaction between two genes: Extension (gene symbol E) and Agouti (gene symbol A).

The gene that controls the distribution pattern of black hair is known as A. The allele A in combination with E will confine the black hair to the points to produce a bay (Fig. 1G). Various shades of bay from brown, dark bay through mahogany bay, blood bay to copper bay and light bay exist. The genetics of these variations has not been defined. Any bay horse will include A and E in its genetic formula as well as ww and gg.

Black pigmented horses (black, bay, brown, buckskin and grullo, to name a few) have at least one E allele.

Red Factor results are reported as E/e Both black and red factors detected. The horse can be assumed to be heterozygous for the red factor (Ee). It can transmit either E or e to its offspring. The basic color of the horse will be black, bay or brown, but depending on genes at other color loci, the horse may be buckskin, zebra dun, grullo, perlino, gray, white or any of these colors with the white hair patterns tobiano, overo, roan or appaloosa.

[Mellifluous]

There is no such thing as At or A+ - there is no test for it because it does not exist.

Agouti only has has two alleles.

Brown has not been found/proven yet. It is accepted that there are brown horses, we just don't know how to differentiate them from bay horses genetically just yet. Like I said we know it is there, like we knew about dun but up until recently dun could not be tested for/proven.

[paintedhorizon]

Mel, (NOT challenging here, honestly asking) how do you know brown hasn't been found/proven yet?

[paintedhorizon]

I have sent them an email asking where this test is.Good point - please do give sources for your information. And tell us if the gene/s is proposed or verified.

This came from horsecolor.com BUT although it says the brown gene has a test it doesn't say who does it.

Brown (AtAt or Ata, plus EE or Ee)

http://www.horsecolor.com/images/brown_sm.jpg (http://www.horsecolor.com/images/brown.jpg)There is now a DNA test to differentiate this color from bay or black. It's definitely a separate and distinct color meriting a category of its own. The color is called "black and tan" in some countries, which is an apt description. The basic appearance is that of a black horse with tan highlights in specific areas -- the muzzle, flanks, underbelly, and girth areas. The darkest shades of seal brown would be almost all black except for a little tan at the muzzle and flank, while the lighter ones look more like a tan horse with an overlay of black covering a good deal of the body, and the very lightest shades of seal brown might look very much like some bays. At one time a theory was proposed that seal brown was caused by a solid black base color with a 'pangare' gene, however, this theory was disproved when the a allele was isolated and a test for it developed -- since none of the seal browns that have been tested turned out to be aa, they could not be "black plus" anything.


It also doesn't give a source for this information.

[Mellifluous]

The closest thing you have to a brown test is the guy from PetDNA doing a study on what he is calling At which is a single marker that he found close to agouti. I think he will do research testing but it is not offered as an official test as it is only one marker and has a 95% accuracy rate. What you end up with is a shaky test based on only one marker that has a 5% error off the bat.

UC Davis waited until they had found many markers associated with Dun before offering the zygosity test and still are not offering it as an outright dun test.

[Siggy]

so it is like the tobiano test, you can not test a horse for 1 tobiano pinto gene but can test for zygosity. I wonder how long until the horse genome is mapped?

[lisa l aka marci]

You guys are worried about brown and our association still lists _albino_ as a color and lists 27 horses as albino..... the first one on the list is from a dun and a buckskin....


How about an albino from a roan and a buckskin????? - Is that possible?

[motorgypsy]

There is supposed to be a dominant white but no albino horses. Horses that are registered as albino in PFHA are cremellos or perlinos - double creme dilution on base E black or e red horses. Maria Luisa is one in our pedigrees that is obviously a double creme dilute, not an albino as she produced palominos and buckskins. Albinos are generally recessive also so if you breed a true albino to a non albino, the color of the non albino will prevail and there will be no evidence of an albino parent. Albino is not a co dominance or incomplete dominance gene. Obviously at some point in the history of the horse a true albino could have existed but the offspring of those labeled albino by PFHA show by the colors of their offspring and parents that they are not albino.

The horse has been mapped but this article explains what is going on now.

http://www.avma.org/onlnews/javma/apr07/070401n.asp

more sources

http://www.ncbi.nlm.nih.gov/sites/entrez?Db=genomeprj&cmd=ShowDetailView&TermToSearch=11765

UCDavis and genome project

http://www.vgl.ucdavis.edu/genomic/

one more that tells you about the actual horse that was mapped

http://www.nih.gov/news/pr/feb2007/nhgri-07.htm

[Siggy]

sorry - I should have said genome identify actual markers. I had heard of this and read it a few years ago. Interesting to read, I am going to look for updated info from when I last read it.

[SandyMM]

How about an albino from a roan and a buckskin????? - Is that possible?
My guess is...... uh, no! Just proves that there are unverified pedigrees....

[motorgypsy]

This is the link
http://www.ncbi.nlm.nih.gov/mapview/maps.cgi?taxid=9796&chr=1&MAPS=ugSsc,ugOar,ugHs,ugBt-r&cmd=focus&fill=80&query=uid(4288436,4287501,4287031,4286039,4283228, 4273105,4263976,4262442,4259952,4258299,4258105,42 54263,4251610,4250944,4250450,4249097,4247457,4245 755,4245393,4243869)&QSTR=gene (http://www.ncbi.nlm.nih.gov/mapview/maps.cgi?taxid=9796&chr=1&MAPS=ugSsc,ugOar,ugHs,ugBt-r&cmd=focus&fill=80&query=uid%284288436,4287501,4287031,4286039,428322 8,4273105,4263976,4262442,4259952,4258299,4258105, 4254263,4251610,4250944,4250450,4249097,4247457,42 45755,4245393,4243869%29&QSTR=gene)

Here is chromosome 1 with descriptions
It won't copy like the original but the brackets correspond to the description down below in order.

From what I understand they are in particular looking for correspondence to human genes and again in particular those associated with inherited problems in humans and other species that have already been mapped I suppose.

Equus caballus (horse) (http://www.ncbi.nlm.nih.gov/genome/guide/horse/) Build 1.1 (http://www.ncbi.nlm.nih.gov/mapview/stats/BuildStats.cgi?taxid=9796&build=1&ver=1) BLAST Horse Sequences (http://www.ncbi.nlm.nih.gov/genome/seq/BlastGen/BlastGen.cgi?taxid=9796) Chromosome: [ 1 ] 2 (http://javascript%3Cb%3E%3C/b%3E:self_to%28%27&MAPS=ugSsc,ugOar,ugHs,ugBt-r&CHR=2%27,%5B%27maps%27,%27chr%27%5D%29) 3 (http://javascript%3Cb%3E%3C/b%3E:self_to%28%27&MAPS=ugSsc,ugOar,ugHs,ugBt-r&CHR=3%27,%5B%27maps%27,%27chr%27%5D%29) 4 (http://javascript%3Cb%3E%3C/b%3E:self_to%28%27&MAPS=ugSsc,ugOar,ugHs,ugBt-r&CHR=4%27,%5B%27maps%27,%27chr%27%5D%29) 5 (http://javascript%3Cb%3E%3C/b%3E:self_to%28%27&MAPS=ugSsc,ugOar,ugHs,ugBt-r&CHR=5%27,%5B%27maps%27,%27chr%27%5D%29) 6 (http://javascript%3Cb%3E%3C/b%3E:self_to%28%27&MAPS=ugSsc,ugOar,ugHs,ugBt-r&CHR=6%27,%5B%27maps%27,%27chr%27%5D%29) 7 (http://javascript%3Cb%3E%3C/b%3E:self_to%28%27&MAPS=ugSsc,ugOar,ugHs,ugBt-r&CHR=7%27,%5B%27maps%27,%27chr%27%5D%29) 8 (http://javascript%3Cb%3E%3C/b%3E:self_to%28%27&MAPS=ugSsc,ugOar,ugHs,ugBt-r&CHR=8%27,%5B%27maps%27,%27chr%27%5D%29) 9 (http://javascript%3Cb%3E%3C/b%3E:self_to%28%27&MAPS=ugSsc,ugOar,ugHs,ugBt-r&CHR=9%27,%5B%27maps%27,%27chr%27%5D%29) 10 (http://javascript%3Cb%3E%3C/b%3E:self_to%28%27&MAPS=ugSsc,ugOar,ugHs,ugBt-r&CHR=10%27,%5B%27maps%27,%27chr%27%5D%29) 11 (http://javascript%3Cb%3E%3C/b%3E:self_to%28%27&MAPS=ugSsc,ugOar,ugHs,ugBt-r&CHR=11%27,%5B%27maps%27,%27chr%27%5D%29) 12 (http://javascript%3Cb%3E%3C/b%3E:self_to%28%27&MAPS=ugSsc,ugOar,ugHs,ugBt-r&CHR=12%27,%5B%27maps%27,%27chr%27%5D%29) 13 (http://javascript%3Cb%3E%3C/b%3E:self_to%28%27&MAPS=ugSsc,ugOar,ugHs,ugBt-r&CHR=13%27,%5B%27maps%27,%27chr%27%5D%29) 14 (http://javascript%3Cb%3E%3C/b%3E:self_to%28%27&MAPS=ugSsc,ugOar,ugHs,ugBt-r&CHR=14%27,%5B%27maps%27,%27chr%27%5D%29) 15 (http://javascript%3Cb%3E%3C/b%3E:self_to%28%27&MAPS=ugSsc,ugOar,ugHs,ugBt-r&CHR=15%27,%5B%27maps%27,%27chr%27%5D%29) 16 (http://javascript%3Cb%3E%3C/b%3E:self_to%28%27&MAPS=ugSsc,ugOar,ugHs,ugBt-r&CHR=16%27,%5B%27maps%27,%27chr%27%5D%29) 17 (http://javascript%3Cb%3E%3C/b%3E:self_to%28%27&MAPS=ugSsc,ugOar,ugHs,ugBt-r&CHR=17%27,%5B%27maps%27,%27chr%27%5D%29) 18 (http://javascript%3Cb%3E%3C/b%3E:self_to%28%27&MAPS=ugSsc,ugOar,ugHs,ugBt-r&CHR=18%27,%5B%27maps%27,%27chr%27%5D%29) 19 (http://javascript%3Cb%3E%3C/b%3E:self_to%28%27&MAPS=ugSsc,ugOar,ugHs,ugBt-r&CHR=19%27,%5B%27maps%27,%27chr%27%5D%29) 20 (http://javascript%3Cb%3E%3C/b%3E:self_to%28%27&MAPS=ugSsc,ugOar,ugHs,ugBt-r&CHR=20%27,%5B%27maps%27,%27chr%27%5D%29) 21 (http://javascript%3Cb%3E%3C/b%3E:self_to%28%27&MAPS=ugSsc,ugOar,ugHs,ugBt-r&CHR=21%27,%5B%27maps%27,%27chr%27%5D%29) 22 (http://javascript%3Cb%3E%3C/b%3E:self_to%28%27&MAPS=ugSsc,ugOar,ugHs,ugBt-r&CHR=22%27,%5B%27maps%27,%27chr%27%5D%29) 23 (http://javascript%3Cb%3E%3C/b%3E:self_to%28%27&MAPS=ugSsc,ugOar,ugHs,ugBt-r&CHR=23%27,%5B%27maps%27,%27chr%27%5D%29) 24 (http://javascript%3Cb%3E%3C/b%3E:self_to%28%27&MAPS=ugSsc,ugOar,ugHs,ugBt-r&CHR=24%27,%5B%27maps%27,%27chr%27%5D%29) 25 (http://javascript%3Cb%3E%3C/b%3E:self_to%28%27&MAPS=ugSsc,ugOar,ugHs,ugBt-r&CHR=25%27,%5B%27maps%27,%27chr%27%5D%29) 26 (http://javascript%3Cb%3E%3C/b%3E:self_to%28%27&MAPS=ugSsc,ugOar,ugHs,ugBt-r&CHR=26%27,%5B%27maps%27,%27chr%27%5D%29) 27 (http://javascript%3Cb%3E%3C/b%3E:self_to%28%27&MAPS=ugSsc,ugOar,ugHs,ugBt-r&CHR=27%27,%5B%27maps%27,%27chr%27%5D%29) 28 (http://javascript%3Cb%3E%3C/b%3E:self_to%28%27&MAPS=ugSsc,ugOar,ugHs,ugBt-r&CHR=28%27,%5B%27maps%27,%27chr%27%5D%29) 29 (http://javascript%3Cb%3E%3C/b%3E:self_to%28%27&MAPS=ugSsc,ugOar,ugHs,ugBt-r&CHR=29%27,%5B%27maps%27,%27chr%27%5D%29) 30 (http://javascript%3Cb%3E%3C/b%3E:self_to%28%27&MAPS=ugSsc,ugOar,ugHs,ugBt-r&CHR=30%27,%5B%27maps%27,%27chr%27%5D%29) 31 (http://javascript%3Cb%3E%3C/b%3E:self_to%28%27&MAPS=ugSsc,ugOar,ugHs,ugBt-r&CHR=31%27,%5B%27maps%27,%27chr%27%5D%29) X (http://javascript%3Cb%3E%3C/b%3E:self_to%28%27&MAPS=ugSsc,ugOar,ugHs,ugBt-r&CHR=X%27,%5B%27maps%27,%27chr%27%5D%29) Y MT (http://javascript%3Cb%3E%3C/b%3E:self_to%28%27&MAPS=ugSsc,ugOar,ugHs,ugBt-r&CHR=MT%27,%5B%27maps%27,%27chr%27%5D%29) Query: gene [clear] (http://javascript%3Cb%3E%3C/b%3E:self_to%28%27%27,%5B%27query%27,%27qstr%27,%2 7rid%27,%27query_number%27,%27remote%27%5D%29;) Master Map: Bos taurus UniGene Clusters Summary of Maps (http://www.ncbi.nlm.nih.gov/mapview/maps.cgi?taxid=9796&chr=1&MAPS=ugSsc,ugOar,ugHs,ugBt-r&cmd=focus&fill=80&query=uid%284288436,4287501,4287031,4286039,428322 8,4273105,4263976,4262442,4259952,4258299,4258105, 4254263,4251610,4250944,4250450,4249097,4247457,42 45755,4245393,4243869%29&QSTR=gene#summary) http://www.ncbi.nlm.nih.gov/mapview/static/mapsnoptions.gif (http://javascript%3Cb%3E%3C/b%3E:%20void%20display_settings%28%29) Region Displayed: 0-180M bp Download/View Sequence/Evidence (http://www.ncbi.nlm.nih.gov/mapview/seq_reg.cgi?taxid=9796&chr=1&from=1&to=179667691&QSTR=gene&QUERY=uid%284288436,4287501,4287031,4286039,428322 8,4273105,4263976,4262442,4259952,4258299,4258105, 4254263,4251610,4250944,4250450,4249097,4247457,42 45755,4245393,4243869%29) http://www.ncbi.nlm.nih.gov/corehtml/spacer10.GIF http://www.ncbi.nlm.nih.gov/projects/mapview/maps.cgi?taxid=9796&chr=1&MAPS=ugSsc,ugOar,ugHs,ugBt-r&cmd=focus&fill=80&query=uid%284288436,4287501,4287031,4286039,428322 8,4273105,4263976,4262442,4259952,4258299,4258105, 4254263,4251610,4250944,4250450,4249097,4247457,42 45755,4245393,4243869%29&QSTR=gene&GIF=maps%280%29&HKEY=NCID_01_1183943_130.14.22.110_9001_1211996018

[motorgypsy]

These are the corresponding discriptions for the above brackets. it wouldn't let me put them all on one page.

Hits:UniGeneSymbolDescription
13:Bt.35465 (http://www.ncbi.nlm.nih.gov/UniGene/clust.cgi?ORG=Bt&CID=35465)LOC534925Similar to RIKEN cDNA 2010208K18 gene
2:Bt.95222 (http://www.ncbi.nlm.nih.gov/UniGene/clust.cgi?ORG=Bt&CID=95222)LOC615557Similar to RIKEN cDNA A930008G19 gene
40:Bt.20288 (http://www.ncbi.nlm.nih.gov/UniGene/clust.cgi?ORG=Bt&CID=20288)MGC179374Similar to nuclear factor of kappa light polypeptide gene enhancer in B-cell...
40:Bt.50069 (http://www.ncbi.nlm.nih.gov/UniGene/clust.cgi?ORG=Bt&CID=50069)SAR1ASAR1 gene homolog A (S. cerevisiae)
25:Bt.14219 (http://www.ncbi.nlm.nih.gov/UniGene/clust.cgi?ORG=Bt&CID=14219)MGC140248Similar to fasting induced gene
31:Bt.25603 (http://www.ncbi.nlm.nih.gov/UniGene/clust.cgi?ORG=Bt&CID=25603)MGC152409Similar to RIKEN cDNA 2210412D01 gene
1:Bt.7742 (http://www.ncbi.nlm.nih.gov/UniGene/clust.cgi?ORG=Bt&CID=7742)MGC152214Similar to gamma tubulin ring complex protein (76p gene)
5:Bt.45929 (http://www.ncbi.nlm.nih.gov/UniGene/clust.cgi?ORG=Bt&CID=45929)MGC148433Similar to RIKEN cDNA C630028N24 gene
7:Bt.24486 (http://www.ncbi.nlm.nih.gov/UniGene/clust.cgi?ORG=Bt&CID=24486)LOC532938Similar to bright and dead ringer gene product homologous protein Bdp
36:Bt.3196 (http://www.ncbi.nlm.nih.gov/UniGene/clust.cgi?ORG=Bt&CID=3196)STRA6Stimulated by retinoic acid gene 6 homolog
2:Bt.82256 (http://www.ncbi.nlm.nih.gov/UniGene/clust.cgi?ORG=Bt&CID=82256)LOC787358Similar to RIKEN cDNA 4930425N13 gene
22:Bt.46603 (http://www.ncbi.nlm.nih.gov/UniGene/clust.cgi?ORG=Bt&CID=46603)LOC785001Similar to RIKEN cDNA 4930425N13 gene
904:Bt.40497 (http://www.ncbi.nlm.nih.gov/UniGene/clust.cgi?ORG=Bt&CID=40497)PKM2Pyruvate kinase 3
1389:Bt.8125 (http://www.ncbi.nlm.nih.gov/UniGene/clust.cgi?ORG=Bt&CID=8125)RPLP1Ribosomal protein, large, P1
1273:Bt.62354 (http://www.ncbi.nlm.nih.gov/UniGene/clust.cgi?ORG=Bt&CID=62354)LOC507271Similar to ribosomal protein L4
42:Bt.27184 (http://www.ncbi.nlm.nih.gov/UniGene/clust.cgi?ORG=Bt&CID=27184)KIAA0377Similar to a putative C.elegans gene encoded in cosmid F46F11
28:Bt.7742 (http://www.ncbi.nlm.nih.gov/UniGene/clust.cgi?ORG=Bt&CID=7742)MGC152214Similar to gamma tubulin ring complex protein (76p gene)
9:Bt.61724 (http://www.ncbi.nlm.nih.gov/UniGene/clust.cgi?ORG=Bt&CID=61724)LOC538143Similar to ras homolog gene family, member V
96:Bt.55928 (http://www.ncbi.nlm.nih.gov/UniGene/clust.cgi?ORG=Bt&CID=55928)MGC142812Similar to gene model 631, (NCBI) (predicted)
74:Bt.9027 (http://www.ncbi.nlm.nih.gov/UniGene/clust.cgi?ORG=Bt&CID=9027)NFKBIANuclear factor of kappa light polypeptide gene enhancer in B-cells inhibitor...

[motorgypsy]

I did find this. Don't know if it's the right one but it's on chromosome 3. Description is at the bottom. It's near the top of chromosome 3 but they only show the section where it's located

http://www.ncbi.nlm.nih.gov/projects/mapview/maps.cgi?taxid=9796&chr=3&MAPS=genes-r&cmd=focus&fill=80&query=uid(3453477)&QSTR=agouti%20equine (http://www.ncbi.nlm.nih.gov/projects/mapview/maps.cgi?taxid=9796&chr=3&MAPS=genes-r&cmd=focus&fill=80&query=uid%283453477%29&QSTR=agouti%20equine)
http://www.ncbi.nlm.nih.gov/corehtml/spacer10.GIF Equus caballus (horse) (http://www.ncbi.nlm.nih.gov/genome/guide/horse/) Build 1.1 (http://www.ncbi.nlm.nih.gov/projects/mapview/stats/BuildStats.cgi?taxid=9796&build=1&ver=1) BLAST Horse Sequences (http://www.ncbi.nlm.nih.gov/genome/seq/BlastGen/BlastGen.cgi?taxid=9796) Chromosome: 1 (http://javascript%3Cb%3E%3C/b%3E:self_to%28%27&MAPS=genes-r&CHR=1%27,%5B%27maps%27,%27chr%27%5D%29) 2 (http://javascript%3Cb%3E%3C/b%3E:self_to%28%27&MAPS=genes-r&CHR=2%27,%5B%27maps%27,%27chr%27%5D%29) [ 3 ] 4 (http://javascript%3Cb%3E%3C/b%3E:self_to%28%27&MAPS=genes-r&CHR=4%27,%5B%27maps%27,%27chr%27%5D%29) 5 (http://javascript%3Cb%3E%3C/b%3E:self_to%28%27&MAPS=genes-r&CHR=5%27,%5B%27maps%27,%27chr%27%5D%29) 6 (http://javascript%3Cb%3E%3C/b%3E:self_to%28%27&MAPS=genes-r&CHR=6%27,%5B%27maps%27,%27chr%27%5D%29) 7 (http://javascript%3Cb%3E%3C/b%3E:self_to%28%27&MAPS=genes-r&CHR=7%27,%5B%27maps%27,%27chr%27%5D%29) 8 (http://javascript%3Cb%3E%3C/b%3E:self_to%28%27&MAPS=genes-r&CHR=8%27,%5B%27maps%27,%27chr%27%5D%29) 9 (http://javascript%3Cb%3E%3C/b%3E:self_to%28%27&MAPS=genes-r&CHR=9%27,%5B%27maps%27,%27chr%27%5D%29) 10 (http://javascript%3Cb%3E%3C/b%3E:self_to%28%27&MAPS=genes-r&CHR=10%27,%5B%27maps%27,%27chr%27%5D%29) 11 (http://javascript%3Cb%3E%3C/b%3E:self_to%28%27&MAPS=genes-r&CHR=11%27,%5B%27maps%27,%27chr%27%5D%29) 12 (http://javascript%3Cb%3E%3C/b%3E:self_to%28%27&MAPS=genes-r&CHR=12%27,%5B%27maps%27,%27chr%27%5D%29) 13 (http://javascript%3Cb%3E%3C/b%3E:self_to%28%27&MAPS=genes-r&CHR=13%27,%5B%27maps%27,%27chr%27%5D%29) 14 (http://javascript%3Cb%3E%3C/b%3E:self_to%28%27&MAPS=genes-r&CHR=14%27,%5B%27maps%27,%27chr%27%5D%29) 15 (http://javascript%3Cb%3E%3C/b%3E:self_to%28%27&MAPS=genes-r&CHR=15%27,%5B%27maps%27,%27chr%27%5D%29) 16 (http://javascript%3Cb%3E%3C/b%3E:self_to%28%27&MAPS=genes-r&CHR=16%27,%5B%27maps%27,%27chr%27%5D%29) 17 (http://javascript%3Cb%3E%3C/b%3E:self_to%28%27&MAPS=genes-r&CHR=17%27,%5B%27maps%27,%27chr%27%5D%29) 18 (http://javascript%3Cb%3E%3C/b%3E:self_to%28%27&MAPS=genes-r&CHR=18%27,%5B%27maps%27,%27chr%27%5D%29) 19 (http://javascript%3Cb%3E%3C/b%3E:self_to%28%27&MAPS=genes-r&CHR=19%27,%5B%27maps%27,%27chr%27%5D%29) 20 (http://javascript%3Cb%3E%3C/b%3E:self_to%28%27&MAPS=genes-r&CHR=20%27,%5B%27maps%27,%27chr%27%5D%29) 21 (http://javascript%3Cb%3E%3C/b%3E:self_to%28%27&MAPS=genes-r&CHR=21%27,%5B%27maps%27,%27chr%27%5D%29) 22 (http://javascript%3Cb%3E%3C/b%3E:self_to%28%27&MAPS=genes-r&CHR=22%27,%5B%27maps%27,%27chr%27%5D%29) 23 (http://javascript%3Cb%3E%3C/b%3E:self_to%28%27&MAPS=genes-r&CHR=23%27,%5B%27maps%27,%27chr%27%5D%29) 24 (http://javascript%3Cb%3E%3C/b%3E:self_to%28%27&MAPS=genes-r&CHR=24%27,%5B%27maps%27,%27chr%27%5D%29) 25 (http://javascript%3Cb%3E%3C/b%3E:self_to%28%27&MAPS=genes-r&CHR=25%27,%5B%27maps%27,%27chr%27%5D%29) 26 (http://javascript%3Cb%3E%3C/b%3E:self_to%28%27&MAPS=genes-r&CHR=26%27,%5B%27maps%27,%27chr%27%5D%29) 27 (http://javascript%3Cb%3E%3C/b%3E:self_to%28%27&MAPS=genes-r&CHR=27%27,%5B%27maps%27,%27chr%27%5D%29) 28 (http://javascript%3Cb%3E%3C/b%3E:self_to%28%27&MAPS=genes-r&CHR=28%27,%5B%27maps%27,%27chr%27%5D%29) 29 (http://javascript%3Cb%3E%3C/b%3E:self_to%28%27&MAPS=genes-r&CHR=29%27,%5B%27maps%27,%27chr%27%5D%29) 30 (http://javascript%3Cb%3E%3C/b%3E:self_to%28%27&MAPS=genes-r&CHR=30%27,%5B%27maps%27,%27chr%27%5D%29) 31 (http://javascript%3Cb%3E%3C/b%3E:self_to%28%27&MAPS=genes-r&CHR=31%27,%5B%27maps%27,%27chr%27%5D%29) X (http://javascript%3Cb%3E%3C/b%3E:self_to%28%27&MAPS=genes-r&CHR=X%27,%5B%27maps%27,%27chr%27%5D%29) Y MT (http://javascript%3Cb%3E%3C/b%3E:self_to%28%27&MAPS=genes-r&CHR=MT%27,%5B%27maps%27,%27chr%27%5D%29) Query: agouti equine [clear] (http://javascript%3Cb%3E%3C/b%3E:self_to%28%27%27,%5B%27query%27,%27qstr%27,%2 7rid%27,%27query_number%27,%27remote%27%5D%29;) Master Map: Genes On Sequence Summary of Maps (http://www.ncbi.nlm.nih.gov/projects/mapview/maps.cgi?taxid=9796&chr=3&MAPS=genes-r&cmd=focus&fill=80&query=uid%283453477%29&QSTR=agouti%20equine#summary) http://www.ncbi.nlm.nih.gov/projects/mapview/static/mapsnoptions.gif (http://javascript%3Cb%3E%3C/b%3E:%20void%20display_settings%28%29) Region Displayed: 17,852,880-17,853,840 bp Download/View Sequence/Evidence (http://www.ncbi.nlm.nih.gov/projects/mapview/seq_reg.cgi?taxid=9796&chr=3&from=17852882&to=17853836&QSTR=agouti%20equine&QUERY=uid%283453477%29) http://www.ncbi.nlm.nih.gov/corehtml/spacer10.GIF http://www.ncbi.nlm.nih.gov/projects/mapview/maps.cgi?taxid=9796&chr=3&MAPS=genes-r&cmd=focus&fill=80&query=uid%283453477%29&QSTR=agouti%20equine&GIF=maps%280%29&HKEY=NCID_01_4336163_130.14.22.95_9001_1211997124
SymbolO (http://www.ncbi.nlm.nih.gov/projects/mapview/static/MapViewerHelp.html#Orientation)Links (http://www.ncbi.nlm.nih.gov/projects/mapview/static/MapViewerHelp.html#Links)E (http://www.ncbi.nlm.nih.gov/projects/mapview/static/MapViewerHelp.html#Evidence)Description



LOC100066082 (http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=gene&cmd=retrieve&dopt=full_report&list_uids=100066082)http://www.ncbi.nlm.nih.gov/projects/mapview/static/mstrand.gifsv (http://www.ncbi.nlm.nih.gov/entrez/viewer.fcgi?view=graph&val=NW_001799711.1&_gene=LOC100066082)pr (http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=gene&cmd=Display&dopt=gene_protein&from_uid=100066082)dl (http://www.ncbi.nlm.nih.gov/projects/mapview/seq_reg.cgi?taxid=9796&chr=3&from=17852978&to=17853741)ev (http://www.ncbi.nlm.nih.gov/sutils/evv.cgi?taxid=9796&contig=NW_001799711.1&gene=LOC100066082&lid=100066082)mm (http://www.ncbi.nlm.nih.gov/projects/mapview/modelmaker.cgi?taxid=9796&contig=NW_001799711.1&gene=LOC100066082)
sts (http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=gene&cmd=Display&dopt=gene_unists&from_uid=100066082)proteinsimilar to Agouti related protein

[paintedhorizon]

Huh? I'm lost. LOL

[paintedhorizon]

Heard back from my friend.

A lot of the information is proven, while some is theoretical based on breeding evidence and research. For example, extension, agouti, creme, champagne, pearl, dun, tobiano, grey, sabino-1, frame, dominant white and silver are all mapped and proven. Pangare, flaxen, sooty, splash, rabicano, seal, and appy colors are all theories, some stronger than others.

I graduated from Washington State Univ with a bachelors in Animal Science and currently attend WSU College of Vet Med.

I started doing more research into and since have been reading the published scientific papers and research.

[motorgypsy]

For non science people the horse has 32 pairs chromosomes that make its heredity. A Chromosome is a long strand of DNA that looks like a twisted ladder made of two strands connected by certain chemicals like the rungs of a ladder and is made of only certain chemicals and the type, number and order of these chemicals determine what the individual will be like. To study it the two strands are disconnected by chemicals in a lab and analyzed. If you know the composition of one side of the ladder, you also know the other side because only certain chemicals stick together.

One half the total set of pairs comes from dam and one half of the total set from sire and they combine when an egg is fertilized to produce the new individual. But it's not that simple because they can get switched around when the sex cells are produced by the parents. If it were that simple there would be only 4 possible types of offspring from two parents - which of course there aren't.

The jagged vertical line pictures with labels on them represent the chemicals in part of a particular horse chromosome and the trait the small groups of the chemicals produce. Many are referenced to already known sections of the chromosomes of other species like rat or human or mouse which is why most of the labels don't make sense unless you are very familiar with what they are referring to.

I posted the diagrams because it's interesting to see exactly what people working in this field look at and how they represent what they find. Only those who work directly in the field understand what the labels mean. I've actually separated DNA myself as has Kyle but I don't know specifically what the labels refer to on the diagrams.

Hope this helps. Please add or correct if you see a need.

[Rusel]

No matter what the color.....that Tante is one fine piece of horse flesh...!!! I have a nice appy looking of someone like that...!!!!

[paintedhorizon]

MG, heard from the lady at that website you found. This is what she said.

The seal brown allele at the agouti locus was fairly recently discovered by Michal Prochazka at PetDNA Services in AZ. Their website is here: http://www.petdnaservicesaz.com/Equine.html I don't know if there's any info on there yet about the seal brown test, but you can order one if you have a horse that you want to test.

[Mellifluous]

Yup, that is the guy I mentioned earlier in the thread.

[motorgypsy]

I'm from Missouri. I want documentation from a research equine geneticist and a write up in a scientific magazine before I pay for the test;)

[paintedhorizon]

I think he's legit.
We are a Licensed and Registered independent Laboratory. Our Founder/Director has over 20 years expertise in DNA testing, and is an author on over 60 peer-reviewed scientfic articles published in professional journals. Please feel free to review his Credentials. Dr. Prochazka is a Member of AFA, NFSS, and several local bird clubs in the sunny Arizona.

MICHAL PROCHAZKA, M.D.

Graduate Education: M.D. Degree (1981), University of Zurich, Switzerland.

Postgraduate Education: Postgraduate Course in Experimental Medicine and Biology. University of Zurich, Switzerland.

Positions as Geneticist: University of Zurich, Switzerland (2 years); The Jackson Laboratory, Bar Harbor, Maine (7 years); National Institutes of Health, Phoenix, Arizona (15 years).

Professional Experience/Skills

Molecular Genetics: Chromosomal mapping and analyses of DNA markers (PCR, SSCP, RFLP, AFLP); determination of exon-intron structure of genes, and identification of new polymorphic markers; scanning of genomic DNA for mutations; development of DNA tests; large scale DNA marker testing; DNA restriction mapping and sequencing.

Laboratory Management: Setting-up a molecular genetics lab; training of staff in molecular genetics techniques; supervising DNA marker testing and mutation screening.

Selected Scientific Publications

Staeheli P, Prochazka M, Steigmeier PA, Haller O. Genetic control of interferon action: Mouse strain distribution and inheritance of an induced protein with guanylate-binding properties. Virology 1984; 137:135-142.
Prochazka M, Staeheli P, Holmes RS, Haller O. Interferon-induced guanylate-binding proteins: Mapping of the murine Gbp-1 locus to chromosome 3. Virology 1985; 145:273-279.
Frater-Schroder M, Prochazka M, Haller O, Arwert F, Porch HJ, Skow LC, Lundin L-G, Hilkens J, Hilgers J. Localization of the gene for the vitamin B12 binding protein, transcobalamin II, near the centromere on mouse chromosome 11, linked to the hemoglobin alpha-chain locus. Biochemical Genetics 1985; 23:139-153.
Leiter EH, Prochazka M, Coleman DL, Serreze DV, Shultz LD. Genetic factors predisposing to diabetes susceptibility in mice. In: The Immunology of Diabetes. Jaworski MA, Mollnar GD, Rajotte RV, Singh B, eds. Elsevier Int. Cong. Series, Amsterdam 1986; Series 717: 29-36.
Prochazka M, Leiter EH, Serreze DV, Coleman DL. Identification of three recessive loci required for insulin-dependent diabetes in non-obese diabetic (NOD) mice. Science 1987; 237: 286-289.
Novak EK, Sweet HO, Prochazka M, Parentis M, Soble R, Reddington M, Cario A, Swank RT. Cocoa: A new mouse model for platelet storage pool deficiency. British Journal of Haematology 1988; 69: 371-378.
Prochazka M, Kozak UC, Kozak LP. A glycerol-3-phosphate dehydrogenase null mutant in BALB/cHeA mice. Journal of Biological Chemistry 1989; 264: 4679-4683.
Shiffer SP, Prochazka M, Jezyk PF, Roderick TH, Yudkoff M, Patterson DF. Organic aciduria and butyryl CoA dehydrogenase deficiency in BALB/cByJ mice. Biochemical Genetics 1989; 27: 47-58.
Prochazka M, Gaskins HR, Leiter EH, Koch-Nolte F, Haag F, Thiele H-G. Chromosomal localization, DNA polymorphism, and expression of Rt-6, the mouse homologue of rat T lymphocyte differentiation marker RT6. Immunogenetics 1991; 33: 152-156.
Prochazka M, Gaskins HR, Shultz LD, Leiter EH. The nonobese diabetic scid mouse: Model for spontaneous thymomagenesis associated with immunodeficiency. Proceedings of the National Academy of Sciences USA 1992; 89: 3290-3294.
Choi MG, Prochazka M, Thuillez P, Lillioja S. A new TaqI allele detected by the CRI-R227 (D4S101) probe in Pima Indians. Nucleic Acids Research 1992; 20: 1157.
Prochazka M, Lillioja S, Tait JF, Knowler WC, Mott DM, Spraul M, Bennett PH, Bogardus C. Linkage of chromosomal markers on 4q with a putative gene determining maximal insulin action in Pima Indians. Diabetes 1993; 42: 514-519.
Mochizuki H, Prochazka M. Dinucleotide repeat polymorphism at the PPP1CA locus on 11q13. Human Molecular Genetics 1994; 3:2265.
Baier LJ, Sacchettini JC, Knowler WC, Eads J, Paolisso G, Tataranni PA, Mochizuki H, Bennett PH, Bogardus C, Prochazka M. An amino acid substitution in the human intestinal fatty acid binding protein is associated with increased fatty acid binding, increased fat oxidation, and insulin resistance. Journal of Clinical Investigation 1995; 95:1281-1287.
Prochazka M, Mochizuki H, Baier LJ, Cohen PTW, Bogardus C. Molecular and linkage analysis of type-1 protein phosphatase catalytic beta-subunit gene: lack of evidence of its major role in insulin resistance in Pima Indians. Diabetologia 1995; 38:461-466.
Ardehali H, Tiller GE, Printz RL, Mochizuki H, Prochazka M, Granner DK. A novel (TA)n polymorphism in the hexokinase II gene: application to noninsulin-dependent diabetes mellitus in the Pima Indians. Human Genetics 1996; 97:482-485.
Prochazka M. Microsatellite hybrid capture technique for simultaneous isolation of various STR markers. Genome Research 1996; 6:646-649.
Rowles JC, Scherer SW, Xi T, Majer M, Nickle DC, Rommens JM, Popov KM, Harris RA, Riebow NL, Xia J, Tsui L-C, Bogardus C, Prochazka M. Cloning and characterization of PDK4 on 7q21.3 encoding a fourth pyruvate dehydrogenase kinase isoenzyme in human. Journal of Biological Chemistry 1996; 271:22376-22382.
Wolford JK, Prochazka M. Structure and expression of the human MTG8/ETO gene. Gene, 1998; 212:103-109.
Mochizuki H, Scherer SW, Xi T, Nickle DC, Majer M, Huizenga JJ, Tsui L-C, Prochazka M. Human PON2 gene at 7q21.3: cloning, multiple mRNA forms, and missense polymorphisms in the coding sequence. Gene, 1998; 213:149-157.
Wolford JK, Bogardus C, Prochazka M. Polymorphism in the 3’ untranslated region of MTG8 is associated with obesity in Pima Indian Males. Biochemical and Biophysical Research Communications 1998; 246:624-626.
Xia J, Scherer SW, Cohen PTW, Majer M, Xi T, Norman RA, Knowler WC, Bogardus C, Prochazka M. A common variant in PPP1R3 associated with insulin resistance and type 2 diabetes. Diabetes 1998; 47:1519-1524.
Wolford JK, Bogardus C, Prochazka M. Genome-wide scan for CAG/CTG repeat expansions in Pimas with early onset of type 2 diabetes mellitus. Molecular Genetics and Metabolism 1999; 66:62-67.
Wolford JK, Bogardus C, Ossowski V, Prochazka M. Molecular characterization of the human PEA15 gene on 1q21-q23 and association with type 2 diabetes mellitus in Pima Indians. Gene 2000; 241:143-148.
Wolford JK, Blunt D, Ballecer C, Prochazka M. High-throughput SNP detection by using DNA pooling and denaturing high performance liquid chromatography (DHPLC). Human Genetics 2000; 107:483-487.
Prochazka M, Walder K, Xia J. AFLP fingerprinting of the human genome. Human Genetics 2001; 108:59-65.
Thameem F, Wolford JK, Bogardus C, Prochazka M. Analysis of PBX1 as a candidate gene for type 2 diabetes mellitus in Pima Indians. Biochimical and Biophysical Acta 2001; 1518:215-220.
Wolford JK, Hanson RL, Kobes S, Bogardus C, Prochazka M. Association of polymorphisms in the KCNJ9 gene with type 2 diabetes mellitus in Pima Indians. Molecular Genetics and Metabolism 2001; 73:97-103.
Wolford JK, Thameem F, Bogardus C, Prochazka M. Molecular analysis of the insulin receptor-related receptor gene (INSRR) on 1q in Pima Indians. Molecular and Cellular Probes 2001; 15:223-227.
Wolford JK, Hanson RL, Bogardus C, Prochazka M. Analysis of the Lamin A/C gene as a candidate for type 2 diabetes susceptibility in Pima Indians. Diabetologia 2001; 44:779-782.
Thameem F, Wolford JK, Wang J, German MS, Bogardus C, Prochazka M. Cloning, expression and genomic structure of human LMX1A, and variant screening in Pima Indians. Gene 2002; 290:217-225.
Farook VS, Bogardus C, Prochazka M. Analysis of MGEA5 on 10q24.1-q24.3 encoding the b-O-linked N-acetylglucosaminidase (O-GLCNAcase) as a candidate gene for type 2 diabetes mellitus in Pima Indians. Molecular Genetics and Metabolism 2002; 77:189-193.
Prochazka M, Farook V, Ossowski V, Wolford JK, Bogardus C. Variant screening of PRKAB2, a type 2 diabetes mellitus susceptibility candidate gene on 1q in Pima Indians. Molecular and Cellular Probes 2002; 16:421-427.
Farook V, Hansen R, Wolford JK, Bogardus C, Prochazka M. Molecular analysis of KCNJ10 on 1q as a candidate gene for type 2 diabetes mellitus in Pima Indians. Diabetes 2002; 51:3342-3346.
Thameem F, Yang X, Permana PA, Wolford JK, Bogardus C, Prochazka M. Evaluation of the microsomal glutathione S-transferase (MGST3) locus on 1q23 as a type 2 diabetes susceptibility gene in Pima Indians. Human Genetics 2003; 113:353-358.
Thameem F, Farook V, Young X, Permana P, Bogardus C, Prochazka M. The transcribed endosulfine a gene (ENSA) is located within a type 2 diabetes-linked region on 1q: sequence and expression analysis in Pima Indians. Molecular Genetics and Metabolism 2004; 81:16-21.

[Mellifluous]

Yes, he is qualified to do genetic testing, etc. It is the test he is conducting that does not have the creds to back it up.

[motorgypsy]

Yup Yup

He can indeed test to see if the marker he is referring to is present or absent but as far as proof that it actually links to black bay - I haven't seen it yet. That doesn't mean it isn't true either but as soon as it is proven to the satisfaction of the other "experts" they will all be offering the test.

[sporthorse]

http://www.pasoregistry.com/db/Profile.asp?ID=70392
would'nt Candida have to be a smoky black coming from a double dilute perlino sire?

[Mellifluous]

what color was her dam? I am guessing black? But yes, it looks like she is a smokey black and she passed on her copy of the cream gene to 25% of her offspring.

[paintedhorizon]

Depends on the color of her dam, but she would at least be Ccrccr since her sire is CcrCcr (cremello)

[motorgypsy]

It says the sire is cremello and that he threw 25% palomino offspring so he had one red gene for sure.

With cremello you don't have a lot of choices for offspring - palomino, buckskin or smokey black. I've never seen a buckskin that dark before although some are really dark but those are usually sooty, not brown colored.

I'd go with smokey black too.

Candida threw a buckskin bred to Coral and I've never heard that he had a creme gene so had to come from her.

[motorgypsy]

SandyM isn't that your Emi that is her son by Coral? He doesn't have a creme gene does he????