C-Notes Sawbuck

[x factor fan]

You might want to try to find a photo of Colourful Gambler, an Australian TB. Seems to have the same expression as Santana horses.

http://www.pedigreequery.com/colourful+gambler

The original mutation seems to have been in the grand dam Glacial. AUS

Looks like each mutations has both different expressions, and different levels of expression. It would be interesting to see if the kind of mutation is similar in both lines.

[rodeoratdogs]

I put in my Yahoo search and found a picture of him on here....lol.
Scroll down a bit....

http://www.allbreedpedigree.com/forum/viewtopic.php?p=10652

I did find out the name of the woman that was doing the research on DW. Her name is Samantha Brooks and she was at the University of Kentucky and now she is at Cornell. So the girl with the horse is going to try to contact her and she if she is still doing the research on DW.

It would be nice if they did have more tests for KIT mutations but I was asking about it the color-info forum and I guess it just wouldn't be cost effective to develop the tests because it's not crucial need to know information like with LWO, so not enough people would test for it to make for the cost of developing the tests.
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[warchief]

I think it's great, all the interest in Sawbuck after all these years.

[whnywriter]

Alicia,

I used the head shot photo of "Sawbuck" in the article I wrote on Nylon for the Paint Horse Journal way back when...sometime in the mid- to late 1990s.

The photo was the only one I've ever seen of him but I'd be willing to bet that Marge Spence has a few more on file. Marge is the wife of former APHA Executive Secretary Sam Ed Spence and she photographed many of the Paint Horse breed's early horses...show and breeding. She did a lot of work for Junior Robertson and Jim Smoot when they were partners.

Marge was a self-taught horse photographer with tons of talent.

Frank Holmes
Kiowa, CO

[rodeoratdogs]

Frank,

Well she found a picture of him, she said it was her "APHA Savy" friend she got it from, she posted on the thread on color-info, here is the link (scroll down a bit). He looks like a young horse in this picture.

http://www.equine-color.info/phpBB3/viewtopic.php?f=22&t=2624&start=50

I got my book today too, thank you!
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[Linda_D]

Okay, I've been lurking on this thread for a while, so I'm finally going to ask the questions that have been spinning around in my brain for a while:

On GQ Santana, is that underlying dark skin that gives him that grayish, "ticking" look? I think his color is listed as chestnut.

Concerning the Patchen line that stems from White Beauty(TB), are they mostly predominantly white horses? I know that White Beauty was, and her descendent The White Fox was, too.

White Beauty and Mont Blanc (in France) were both white TBs foaled in the same year (1963 I think) or one year apart. Another white TB was foaled just three or four years later (can't remember its name). Before that, as far as anyone knows, no white TBs had been foaled since the 1890s. So, why the sudden "explosion" of white TBs in the mid 1960s? Might it have been an environmental factor (like radiation from nuclear testing which was still going on in the early 1960s) that triggered mutations? White Beauty proved that her coloring was genetic as she passed her color on, but I'm not sure if the other white horses (both colts I think) were ever bred.

Any thoughts on these questions?

[rodeoratdogs]

I'll answer part of your question, what you seeing is the pigmented skin though GQ Santana's light coat and yes his base color would be sorrel or chesnut (they are the same genetically "red" or e) because his parents are both sorrel. ee + ee = ee or (red) all horses are either red ee or black EE based, black is dominant over red, two black horses can produce a red horse if they have a recessive red gene Ee, but two red horses can't produce anything but red.

I would say environmental factors had nothing to do with the DW Kit mutations just spacific selective breeding even if by chance. I will let x factor touch more on the TB part since x factor is more familiar with the TB lines.
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[rodeoratdogs]

This is the equine color-info website/forum I belong too, it goes into a lot more explanations on all equine colors....

http://www.equine-color.info/node/19
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[x factor fan]

Just a wild guess, but there probably have been DW mutations all throughout history. In many cultures white horses were considered sacred and suitable sacrifices to the gods. Which of course has the effect of eliminating the DW from the gene pool. Oops, no more white horses.

Another guess is that there probably are lots of DW's in the paint/pinto breeds. Where breeders have been selecting FOR white markings.

Historically TB breeders have selected AGAINST white markings, also dilutes and grays. Part of this is preference, part utility, there was more of a market for solid colors. Easier to match for teams or military units. And of course what would you rather ride on a daring midnight raid? A wildly marked horse with lots of nice white that will show up even in the dark, or a nice solid dark bay, brown, or black?

White foals may have been given away, hiding the presumed impure blood, or even killed right after birth-possible confusion with OWL. Again eliminating them from the gene pool.

Fast forward to the current era of DNA testing--no more suspected fence jumpers when a odd color foal shows up. Modern understanding of genetics, and perhaps best from the horses point of view, no more sacrifice of white horses to ensure a good harvest.

As for your specific question, DW is currently lumping all versions of the KIT mutation under one name. But white they all act in a similar matter, they are different mutations with different levels of change to the KIT gene. Some lines seem to generate mostly white horses--the Patchen line of horses seem to have whites or solids, but not pinto patterns.

Other lines like Puchilligui and Airdrie Apache have some whites, but lots of roany pinto types.

One of the nice things about the Dun Central Station website is that she took the time to do a graphic of each KIT mutation, showing the extent of the mutation.

Hope this answers your questions.

[Linda_D]

Thanks. I've been to the Equine Color site and I'll have to go over to Dun Central.

I understand that nowadays, breeding for white/flashy TBs is much more popular than 50 years ago. However, it just seems a little odd that three white TBs were born within about 3 years of one another and that they weren't hidden away/given away/put down at a time when it would have been likely they would have been. It just makes me wonder if there were sunspots or something that triggered these mutations at about the same time.

[rodeoratdogs]

Just wanted to ad that I talked to someone at Animal genetics (they do all my testing for me) Anyway he said there were 10-12 horses in the Paint's and QH's that had been identified carriers of DW but that there was undoubtedly many more out there, and I don't doubt that.
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[rodeoratdogs]

X-factor,
Doesn't this paragraph explain that DW is indeed Dominant, so therefore it doesn't need to have any other KIT gene to express or were you saying that when combines with another KIT gene that's when you get maximum expression?

The amount of white expressed on a Dominant White animal can range from less than 50% white in some mutations,
to greater than 99% white. Unless another white pattern gene is involved that causes blue eyes, the eyes of a
Dominant White horse are expected to have normal pigment. Dominant White mutations have a dominant mode of
inheritance, as its name suggests. This means that if a horse is heterozygous for Dominant White, they are usually
50% or greater expression of white themselves for most of the documented mutations, and approximately 50% of
their offspring will inherit their mutation.
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[x factor fan]

Take a look at the Puchilingui line horses. Tested to be DW.
Expression ranges from rather minimal look at Sato for example, he looks to have much less than 50% white. To Chet DT and Arctic Squaw, mostly white. All three have DW chromosome from Puchilingui, but there's a range of expression.

Is the range of expression random chance? Or are there other genetic factors involved? I'm coming down on the side of other factors.

It has been pretty well established that base coat color influences white expression. Red based more, black based less.

Jumping to Appaloosa colors for a moment, there seems to be an additive effect with white expression and sabino--the more sabino the more white.

Color breeders have been adding white to increase the chances of a wildly marked foal, so there are a number of horses out there that have DW on one chromosome, and some form of sabino on the other.

Things I've noticed is that the more sabino, the more it boosts other white patterns including DW. Also there may be a connection between the recessive version of Agouti, non-bay (aa) and expression of DW.

Going back to appys for a moment, there are currently two camp. The one gene group, and the two gene crowd. Having looked at the work being done by the Appaloosa project, I'm in the two gene camp. The theory there is that there is a white pattern gene that hides unless the second gene (Lp) is also present in the horse.

This by the way is no more radical than the expression of Bay. Two genes are needed, black base coat, and the Dominant version of Agouti. You can breed horses with black coats to chesnuts and come up with Bays. Happens all the time.

So it doesn't seem to be a big leap in logic to come to the conclusion that there are other genetic factors involved in DW expression.

Since you seem to be pretty up on the genetics, what's your take on the levels of expression?

And back to the Patchen horses. Apparently the owner of the farm dreamed/had a vision/whatever, that he was going to have white TB's. So he was overjoyed when his stallion Ky Colonel sired two white foals out of different mares. I've got a black and white photo of Ky, who looks to be a pretty normal chestnut. He was supposed to have white ticking on his coat and a belly spot--neither shows up in the photo.
This line of horses seem to be either solid or very white, skipping the pinto/paint version.

The whites in Japan from Sunday Silence also seem to be white or solid.

And the Mont Blanc line is alive in Europe, and a white grandson is currently racing.

[rodeoratdogs]

I understand what your saying, but I thought the reason they named DW, DW was because it was a simple dominant not a incomplete dominant. That being said I completely understand what you are saying about level of expression linked to base color, and I'm sure DW could be influenced by other KIT genes but I don't think it has to, do you? is that what you were saying? because that's what I was asking.
I haven't put a whole lot of thought into level of expression linked to base color, but I think it's interesting that the Too cool for you is a minimally marked black sabino/splash and he is consistantly throwing prodominantly white horses linked to red, kind of sneaky of him don't you think? I would like to see what he produced with a EE mare, probably not so much white I bet.

I understand how Agouti works that's why I was excited to find out that my red dun paint mare is aa, I'd really like a grulla foal from her and since she negative for agouti that will be much easier to accomplish as long as I breed her to a DD EE aa stud I just have to find one I like.
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[x factor fan]

Dominant White has to be one of the most confusing names to apply to a color gene. There was a thread over on the TB side about the name and what most folks think of when they hear the name.

Yes, it is dominant. Yes it affects the white markings. But it does not imply that all the horses that carry the gene are pure white.

Jorge suggested the name Stained White. My contribution was Harlequin like the dogs. With the white ones being called White Harlequins, so there could be Black Harlequins, Reds, blues, golds whatever.

Again look at the level of expression between Sato, Chet DT and Arctic Squaw. Same gene at work with 3 different levels of expression.

And it is a dominant because you see some level of expression with only one copy present. And in fact to date no one has found a surviving foal with two copies of the gene.

It might be worth thinking of each mutation with a different name, as they do seem to act slightly differently. Patchen Whites for example.



As for sabino, think of how the genes are linked on each chromosome.

A horse could have one chromosome E (black base coat) Kit normal Kit Roan
and on the other chromosome e(red base coat) Kit Sabino Kit Non-roan.

Carrying two different Kit mutations that don't create an embryonic lethal. But they may have an additive effect when present in the same horse.

It is an interesting problem to sort out.