7 new mutations in KIT found, including two more TB DW!!

Talk about equine color, markings, genetics, etc. Post pictures of flashy Thoroughbreds!

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RiddleMeThis
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Re: Perhaps a dumb question

Postby RiddleMeThis » Wed Jun 03, 2009 7:42 am

soft hearted wrote:If a horse was from one of the above listed DW bloodlines (those identified) and showed some of the characteristics - without actually being largly white, would it still carry the gene and have it be transmissable?
Its possible. They didn't really go into how much white a horse that has dominant white has to have, though they did say something along the lines of normal white markings.
As one of the horses mentioned is now identified as being Dominant White, does that mean they do not carry, nor transmit, any of the previously ascribed sabino genes? (referring to Puchilingui and offspring generationally)
Well, a horse can have more than one white spotting gene. Just because they have dominant white doesn't mean they don't also have sabino as well.
Maybe the better question is - is there a test yet available for submitting to find out without guessing?
Not really. Maybe soon though.

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Postby RiddleMeThis » Wed Jun 03, 2009 7:46 am

summerhorse wrote:I wish they had not named it dom. white because try to explain why a dom. white has 4 socks and a blaze? What we called sabino in TBs is probably all some of these DW mutations. They are just caused by different mutations than the SB1 found in some other breeds that look and act similar but are in different locations.

WHY didn't they just named them sabino 2, 3, 4, 5, etc? It would make life so much easier. :D We always thought "sabino" was not just "one" gene but a whole bunch of them with unknown effects on each other (or without each other).
They called it Dominant White rather than Sabino because ti acts completely different. Dominant White is heterozygous white and homozygous lethal.

Sabino is heterozygous minimal and homozygous white.

They cannot name two things, the same name if the act completely and total different.

It would be like naming Frame Overo and Splash White, Sabino because they can all create white spotting patterns that look similar.

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Postby summerhorse » Thu Jun 04, 2009 1:46 pm

That's why they have numbers!
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Postby RiddleMeThis » Thu Jun 04, 2009 2:53 pm

summerhorse wrote:That's why they have numbers!
No thats NOT why they have numbers. They have numbers because the researchers feel that there are going to be more Sabino patterns, patterns that already fall into the sabino pattern of incomplete dominant. (from the researchers themselves)

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Postby xfactor fan » Sat Jun 06, 2009 7:06 am

It is also possible for a horse to carry Dominant White on one chromosome #3, and Sabino on the other Chromosome #3.

Since base coat also lives on Chromosome #3, it is possible that a horse could carry Black base coat (E) Dominiant White, linked, and carry Red base coat, and sabino on the other chromosome #3. So all the black base coat foals would be DW, and the Red base coat foals sabinos.

Kind of hard to sort them out without testing. A new answer to the old joke "what color was George Washintons white horse?" might be in order.

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Postby Jorge » Sat Jun 06, 2009 6:29 pm

xfactor fan,

Although the following suggested material is not in English, don't miss to browse:

http://www.pedigreequery.com/forum/view ... hp?t=22298

that is:



Dear Members,

For those who would like to understand the definition of various equine coat color Spanish terms, following are two extraordinary references:

01. FIRST REFERENCE -------------------------------------------------------
http://www.oni.escuelas.edu.ar/2001/bs- ... pelass.htm

02. SECOND REFERENCE ----------------------------------------------------
Open the following link:

http://www.search.com/search?q=Overos+M ... rt%C3%ADn+

then open the reference that reads: "PELAJES DE CABALLOS",
that is, "lacautivacaballos.com.ar/trabajos"

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Postby reedhill » Mon Dec 27, 2010 4:55 pm

Big Bump for the author that wrote the BH article to read :shock:

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Postby Jorge » Wed Dec 29, 2010 12:56 pm

After reviewing some of the latest discoveries on our subject topic and some consultation I am beginning to conclude that there may well be many a great number of dissimilar microbiological justifications behind the appearance of every particular white strain within the Thoroughbred breed. That's good news for microbiologists and top notch scientist but not necessarily an assistance for the average horseman/horsewoman who is trying to plan and "predict" the result of his/her humble cross. Applying somehow this rationale to a more common coat color, its like concluding that the "bay" color coming from Nasrullah is different from the "bay" color coming from Dr. Fager. The only difference is that since both lineages are already mixed within the Breed no one bothers now to differentiate both. But since the white color is so rare and scarce within the Breed it can be subdivided into genetic niches, albeit it may take years
of studies. For those reason, the more science let us know their new complicated paradigms the more I see the wisdom behind the phenotypical nomenclatures. I sincerely congratulate scientists for opening to all of us this new vast universe of knowledge, yet I pay tribute to our average breeders for recollecting their centuries-old observations and practical wisdom as per coat color. For those reason I admire some of you breeders, specially cases like that of Dalene Knight, Herman K. Goodpaster and some others.

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Postby RiddleMeThis » Wed Dec 29, 2010 1:05 pm

Jorge wrote:Applying somehow this rationale to a more common coat color, its like concluding that the "bay" color coming from Nasrullah is different from the "bay" color coming from Dr. Fager.
Ugh no it's not. ITs not even REMOTELY similar. The "bay" color is EXACTLY the SAME for EVERY SOURCE. The genetics is the SAME it is the SAME mutation.

The reason the DW are different and all get different numbers is because they ARENT the same. The mutations are DIFFERENT.

For those reason, the more science let us know their new complicated paradigms the more I see the wisdom behind the phenotypical nomenclatures.

No, you just don't understand so choose the easier option.


*refrains from saying more and exploding*
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Postby color » Wed Dec 29, 2010 11:47 pm

RMT

with all this DW mutations, do you understand then WHAT these differences in each of them is and could you explain it, I am getting more and more lost over this DW thing. I am sure others would also like to understand this better by getting it in "normal wording" than in all this scientific language that is even more complicated for me to understand due to being German.

Thanks in advance.
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Postby RiddleMeThis » Thu Dec 30, 2010 12:28 am

This pdf article has a very clear, and very easy to understand explanation of them all.

http://www.duncentralstation.com/PDF/KI ... Castle.pdf

I guess another way to look at it is that they are different mutations, like tobiano and cream are different mutation, but they just happen to create similar looks.

Like sabino roaning can some times look like True Roan.


Does that make it a little clearer?
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Postby angrovestud » Thu Dec 30, 2010 7:11 am

I think its very staight orward and easy to understand, and its quiet easy to see the mutations taking place when you see lines of horses comming together from 2 centuries of paintings and photos.
a ew years ago we went through the same thing with Tobiano they did not have a test for it as it had not been found so science makes breeding easier or it should
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Postby xfactor fan » Thu Dec 30, 2010 1:37 pm

Let me try to do a simple explanation of KIT, and color genetics.

First genetic material is grouped on chromosomes. So all the genes (linked genes) that live on a chromosome will be passed on together.

On equine chromosome #3 base coat color, and a very large gene called KIT.

So each horse will have two chromosome #3's

Chromosome #3--Black (E) --------KIT (no mutations)
Chromosome #3--Red (e) --------KIT (no mutations)

This would be a based horse with no KIT based white markings.


KIT itself with no mutations

ABCDEFGHIJKLMNOPQRSTUV-WXYZ


Kit with the regular roan mutation

ABCDEFGHIJKLMNOPQRSTUV-ZYXW


So a roan horse would be

ABCDEFGHIJKLMNOPQRSTUV-WXYZ
ABCDEFGHIJKLMNOPQRSTUV-ZYXW

A horse with two copies of the roan mutation would be

ABCDEFGHIJKLMNOPQRSTUV-ZYXW
ABCDEFGHIJKLMNOPQRSTUV-ZYXW

And this is a early embryonic lethal.

There is a second roan mutation that when paired with the first roan mutation allows the embryo to develop and be born normal.

ABCDEFGHIJKLMNOPQRSTUV-YZXW

Pure breeding roan

ABCDEFGHIJKLMNOPQRSTUV-ZYXW
ABCDEFGHIJKLMNOPQRSTUV-YZXW

Dominant white is also a KIT mutation.


ABCD-EFGHIJKLMNOPQRSTUV-WXYZ (regular version)


DW 5

ABDC-EFGHIJKLMNOPQRSTUV-WXYZ (DW 5)


ABDC-EFGHIJKLMNOPQRSTUV-WXYZ (DW 5)
ABDC-EFGHIJKLMNOPQRSTUV-WXYZ (DW 5)
Two copies also make a embryonic lethal.


DW 7

BACD-EFGHIJKLMNOPQRSTUV-WXYZ (DW 7)
BACD-EFGHIJKLMNOPQRSTUV-WXYZ (DW 7)
Two copies also make a embryonic lethal.


What is unknown at this time is if

ABDC-EFGHIJKLMNOPQRSTUV-WXYZ (DW 5)
BACD-EFGHIJKLMNOPQRSTUV-WXYZ (DW 7)

Is also a embryonic lethal.

All the versions of DW have slightly different changes in the same region,
so one could be ABDC, another BACD, CDAB, DCAB, BCDA, and so on.

The potential is that each DW mutation will interact with all the other DW mutations in a unique way.

So DW5 X DW7 might be viable, while DW5 x DW9 might not. The only way to tell is for folks to start breeding different lines of DW's together and see what happens.

Since the embryo loss is so early--think failure to implant early--this doesn't result in the heartbreal of a OWL foal, where the foal is born then dies.


So if someone breeds DW5 -regular, to DW7-regular

There should be DW5-DW7, DW5-regular, DW7-regular, regular-regular.

This of course would take lots of breedings to see if one class of horses doesn't appear. And of course someone could get lucky and have a DW5-DW7 show up with the first mating.

Hope this helps.

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Postby RiddleMeThis » Thu Dec 30, 2010 2:11 pm

Roan isn't homozygous embryonic lethal except possibly in a small slew of Brabant Belgians. However the current and most wide spread (AKA APHA AQHA etc etc ) Roan mutation is NOT.

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Postby xfactor fan » Thu Dec 30, 2010 5:17 pm

Ok, but this contradicts everything I've ever read about Roan. Including the breeders who have been seeing a 1:3 ratio instead of a 1:2:1 ratio in roan x roan matings. Roan has kind of been the poster child of early embryonic lethals.


And what they are testing is markers, not the actual roan mutation. If there was a mutation to the roan mutation, it follows that most of the markers would be the same. And until someone finds the actual mutation, there's no telling just how many versions of roan may be out there. DW is up to how many now?


And yes, I could have gone intro the bio-geek speak and talk about Exons and the like, but was trying to provide a over view of how it works to someone that is not a native English speaker, hence the simplifications and examples with roan.