Was Seth Hancock Right About Overbreeding??

[kimberley mine]

As for the large heart gene. Yes, I believe that there is something to the theory. Don't think the large heart gene is the miracle cure all that the X factor books claim. In fact it may make it very difficult for a X factor stallion to be matched with the right kind of mares. -

If the theory is correct, non of the sons will get the large heart, and the extra cardio from the large heart masks what the large heart stallion is going to transmit to his foals.

I would argue that you are correct, in terms of breeding a stallion and hoping that, somewhere down the road, he will have superstar stallion sons. Look at Princequillo, Buckpasser, Secretariat, etc. Better than average sires, average to marginal sires of sires, and exquisite broodmare sires. Also, who were their best offspring? Fillies or colts?

There was a recent discussion about how much Giant's Causeway looks like Rahy, his damsire. This theme keeps coming up with other pairs of horses, where the stallion looks much more like the broodmare sire than his own sire. These observations are coming from folks with an eye for conformation, not folks trying to prove a theory.

How this relates to maternal/paternal chromosome? Don't know, not sure that there has been a lot of research in this area.

I'm not sure if that relates to maternal or paternal chromosones, so much as it relates to how strongly (or not) the mare or stallion is imprinting foals. If every foal the mare throws looks like herself, regardless of sire--then she will be the more dominant force in that mating. Also, if the BM sire is considered to be extremely prepotent, then it should be no surprise if his daughters produce foals that look like him.

[Sysonby]

Re the whole sire versus broodmare sire issue--I'm sure there are sex based factors involved genetically that I am not qualified to discuss. I will note that without fail AFAIK, exceptional broodmare sires covered exceptional mares.

In other words, the apple didn't fall far from the tree. Even if Secretariat wasn't an amazing sire of racehorses overall, he was bred to the best mares around for much of his career. Good broodmares tend to make good broodmares.

[bcassidy]

xfactor fan---I certainly understand the logic of the sex linked gene that could produce a larger heart in an animal. However there is also another theory I would like to put forth (and I am not saying that this is the root cause of the large heart in animals such as Secretariat) that may also help to explain the large heart phenom and it could also be genetically based.
I am aware of a circumstance in which the physical space of the chest cavity (if it is abnormally large) could in fact encourage all the organs within that cavity to enlarge to fill that space, so while the large heart may not be directly attributable to the genes controlling the hearts physical size another set of genes may in fact be contributing to the physical size of the chest cavity which in turn controls the size of all the organs within that cavity. It could also explain why some buyers like to see a deep chest and large girth. The lungs and heart within a large chested animal will enlarge to fill that space and could possibly be very beneficial for an animal which will race.

[xfactor fan]

Hi everybody, I'll try to address the assorted questions that have come up.

Bcassidy: Your memory is excellent. Classic sex linked traits like male pattern baldness, hemophilia, some types of color blindness, just to mention a few are all defective genes carried on the X chromosome. Because the Y is so small, there are large parts of the X that don't have a related region on the Y. So whatever is on the X get expressed.

Imprinting or maternal/paternal chromosome tagging is something else, and is not exclusive to the X and Y chromosomes. Some traits are only expressed when they come from a specific sex parent.


Lets say you have two populations of things. Red things, and White things. You as a budding scientist cross the red things and white things, and look at the next generation. In regular genetics, you can expect to see, either all of the baby things being red, or all of the being white, or pink. Dominant, recessive or Co-Dominant (pink)

Instead you examine your population of baby things, and find that they are a random assortment of white or red. No pinks at all. Very strange.

So you look harder and find that surprise, surprise, the baby things all follow the color of their male parent. So when you cross white males with red females all the baby things are white. Red males crossed with white females result in red babies. That's probably enough Dr. Seuss for now.

At some point in the process a tag is put on the chromosome to identify which parent the chromosome came from, so something, somewhere in the process of cell division keeps track of which parent the chromosome came from and makes the appropriate selections.


kimberley mine & Sysonby
The X factor theory doesn't have much if anything to do with imprinting, and was an answer to the second question from Bcassidy.

The horse breeding folks from the middle east believe that the mare controls the size of the foal. Pre genetic science but acute observers of all things equine.

Leaving out the large heart idea, and broodmare sire ideas, and just looking at conformation, the X may indeed shape the overall structure of the front end of the horse and may determine size.

Take a look at the Princequillo family--not for the large heart, but because they have a distinctive front end, low neck set, thick neck, angle of the withers, and are pretty easy to spot. This family look zig zags from fathers to daughters to grandsons and so on. Secretariat had the family look as did Kris S. So does Storm Cat.

The Man O'War front end is pretty distinctive too, as is the Domino/Sweep/War Admiral front end.

There tend to be good conformation photos of successful racehorses, so this point is often used to support the X factor theory, or broodmare sire theory. But it holds true for less than stellar horses too.

bcassidy:
Consider dogs for a moment. The Irish wolfhound is a huge dog, long of leg, deep of chest, short of life. All of the giant dog breeds suffer from cardiac insufficiency. Not enough heart to pump blood to the giant body. They have a normal dog size heart despite having the room inside the chest cavity to grow a large heart.

There may be a trade off between heart size, and lung function and heart girth, but I don't think this is the primary link with the large hearts that some TB's have.

This view is somewhat colored by knowing a couple of off track TB's with huge heart girths that couldn't run a lick.

My guess, and it is only a guess, is that there is a region on the X chromosome that controls heart size. Let's say one copy of the gene equals a 1 pound heart. Two copies equal 2 lbs and so on with the average horse having 8 copies and a 8 lb heart. Transcription errors when the chromosomes are crossing over could result in one X getting 10 copies of the gene, and the other X getting 6 copies. This matches what vets find when examining and weighing hearts, range of sizes.

I wonder what the average heart size of the giant horse breeds are?

There are examples of the multiple copies of genes in other animals including the "thrill seeking gene" in humans.

[Pan Zareta]

At some point in the process a tag is put on the chromosome to identify which parent the chromosome came from, so something, somewhere in the process of cell division keeps track of which parent the chromosome came from and makes the appropriate selections.

It's genes, not chromosomes, that may be tagged (by adding a methyl group if their function is to be altered). The vast majority of genes in humans and other species that have been studied in this regard have *not* been found to be tagged(imprinted). Those that are tagged tend to be found in clusters. If any tagged genes have been documented in the domestic horse, it's been done very recently. I know someone in the Vet school at Cornell was studying the phenomenon in racing TB's as of 2003.

[Mahubah]

Leaving out the large heart idea, and broodmare sire ideas, and just looking at conformation, the X may indeed shape the overall structure of the front end of the horse and may determine size.

Take a look at the Princequillo family--not for the large heart, but because they have a distinctive front end, low neck set, thick neck, angle of the withers, and are pretty easy to spot. This family look zig zags from fathers to daughters to grandsons and so on. Secretariat had the family look as did Kris S. So does Storm Cat.

The Man O'War front end is pretty distinctive too, as is the Domino/Sweep/War Admiral front end.

Just for the record, would you describe the typical Man o' War and Domino front ends?

[louis finochio]

The only way to track the potency of the sperm is to research the same.

Our the superior runners coming from the 1-50 coverings or are they comin from the 51- 100 coverings? How many 101-200 coverings are productive, great research project.

[xfactor fan]

Pan Zareta

Didn't know that the genes could be tagged too. The papers that I looked at which may have been early research, seemed to be talking about chromosomes, not genes.

Is it possible that on some level both can get tagged?


Mahubah

The Man' O War front end is also pretty easy to spot, they tend to have a high neck set very high withers with an almost flat top. Kind of flat chest, they also tend to be on the tall side. 16 + hands. Spotted Bull might be in the database with a conformation photo.



The Domino/Sweep/War Admiral front end is not as distinctive--has a moderate neck set, not real thick, longish withers, kind of smallish. Over all a very well balanced looking horse.

Sorry about the poor descriptions, words fail when trying to describe a complex combinations of angles that make up horse conformation.


I do have lots of issues with Marianna Haun's research, and especially her conclusions about the Large Heart, but I do think she's spotted something linking the X chromosome and the front end development.

[Pan Zareta]

Pan Zareta

Didn't know that the genes could be tagged too. The papers that I looked at which may have been early research, seemed to be talking about chromosomes, not genes.

Is it possible that on some level both can get tagged?

Tagged as paternal or maternal for purposes of altering or preventing transcription? I don't think so. But in females, at an early point in development most of the genes (all but those in the pseudoautosomal region that *does* recombine w/ the pseudoautosomal region on the Y or the other X) on one X chromosome in each cell of the actual embryo is inactivated, and all the subsequent daughter cells of those cells will have the same X inactivated. Which X gets inactivated is random so ~50% of all cells should have the paternal X active, and ~50% have the maternal X active. This process is controlled by a gene on the X called XIST. The inactivated X can be observed microscopically during interphase as a dark spot in the nucleus & is called the Barr Body.

Interestingly, it is *always* the paternal X that is inactivated in the extraembryonic membranes (those structures that will go on to become the amnion, umbilical cord, and placenta). It may have evolved thusly b/c those structures by necessity interface w/ maternal blood & therefore immune system and keeping them more like Mom helps keep the embryo from being rejected as foreign - but that's just my own speculation.

[mary syers]

Xfactor,
Can you give us a paper to go look up to understand tagging? Mary Syers

[xfactor fan]

Mary,
I'll try to find the papers this weekend, it turned up in a google search when looking for maternal/paternal chromosome info. after reading the article about the sheep with big rears. Tagging in my term not any official designation.

Pan Zareta

A couple of things about X chromosome inactivation. In looking to see what had changed/been discovered/was new/ came across a couple of papers from some guys working with mouse cells. Turns out that they found that the inactivation is not quite so random after all. Some X's were more likely to be the active X.


It didn't take much looking to find examples of this.

Take a look at the nearest tortoiseshell cat. In cats the orange and black gene is on the X. Males are either black or orange. Females can be black, orange or a blend, with the color indicating which is the active X chromosome in that cell.

Calico cats tend to have large patches of white, black and orange, with the black and orange being mostly equal in size.

The tortoiseshell version is mostly black with swirls of orange. Every tortoiseshell cat I've ever seen in person and in photos is mostly black. I've never seen a cat that is mostly orange with swirls of black.

So if X inactivation in cats is random there should be a bell curve distribution of color. With a range from very black, on one end, and very orange on the other, with the bulk showing a mix of orange and black.


So, it sure looks like at least in cats, the black X is more active than the orange X.

Thanks for the info on XIST, didn't know that had be isolated. Genetic science is moving so fast it is hard to keep up with all the new discoveries.

[Mahubah]

Just a thought -- if X inactivation was truly random in the cat, don't think you'd be getting distinct areas of one color or the other either -- wouldn't the "typical" tortie or calico be kind of a brindled color with the black and orange hairs distributed more or less evenly> (That white-patch gene the calicos have must have something to do with why their black/orange patches are so much more distinct than for the torties -- perhaps it also allows more of the orange to be expressed?)

Xfactor, thanks for the description. Basically, from what you're saying, the "Man o' War" front end is the classic Fair Play stayer -- high-headed, big boned, good sweeping shoulder, rangy, capable of carrying weight over a distance. Of course, so many of Fair Play's best had *Rock Sand close up on the damside, so I guess one can argue whence "the look" comes, but Fair Play himself had similar characteristics.

[Pan Zareta]

The pre-eminent practical argument against non-random primary inactivation of one X chromosome in normal (xx) higher-order placental mammalian females is the absence of X-linked pathologies in heterozygotes. It's difficult to extrapolate meaningful X-inactivation data from laboratory species b/c there is considerably more allelic variation on the X in vivo. Just b/c that initial (primary) inactivation is random doesn't mean that all of those original cells will be represented in equal number as the embryo matures. There is some indication in humans of preference for those cell lines carrying whichever X might confer a relative growth advantage [ref. Migeon, B.R., Non random X chromosome inactivation in mammalian cells in Cytogenet Cell Genet. 1998;80(1-4):142-8].

[xfactor fan]

Mahubah,

Just for a giggle take a look at these two photos of Charismatic yearlings from an online sales catalog.
One looks like he's got the Princequillo/Secretariat X, the other doesn't. The fourth or fifth dam in the direct tail female line is by Secretariat. Long way for the X to have travelled.


http://www.obssales.com/images2/Aug171.html


http://www.obssales.com/images2/Aug142.html


As for those pesky cats. One of things that is beginning to show up in online papers is the term "temporal dislocation"
Genes kicking in at different times.

Think of the silver dapple gene in horses. This dilutes black to flaxen. On a bay horse they have light points and mane and tail. However bays are black, that carry the bay gene that lightens the body color to brown.

So it sure looks like the black color is modified to bay first, then the remaining black is modified by the silver flaxen gene. In the other order, silver dapple first then bay, the horse would be flaxen all over.

There could be a couple of things going on with the calico cats. Given the relatively large areas of orange/black patches, it seems like the X inactivation is pretty early. The earlier this happens the larger the resulting area of colored cat skin.

There sure does seem to be a interaction between the white and orange, that the torti's don't have.
Maybe there is temporal dislocation going on with some of the X's, the black x is "fast" the orange is "slow".

Or it could be something else that won't be discovered for years.

Genetic paper links


http://www.genetics.org/cgi/content/abstract/167/3/1525

Non random X inactivation

http://www.genetics.org/cgi/content/full/151/4/1471
chromosome inprinting in bugs

http://www.euchromatin.org/El-Maari01.htm
imprinting


Pan Zareta,

Most of the papers that showed up in the google did mention the genes being tagged rather than the chromosomes. However some clearly seem to be talking about the chromosomes. It may be that both occure, or perhaps it depends on the methods used by the labs. Some may have the technology to look at genes, others may be looking for movement of the chromosomes.

In either case the "tagging" is a read/write segment that gets marked and erased during reduction division.

[JCBloodstock]

[quote="BJ"] How many mega horses were bred at the 188th breeding???

Not meaning to offend here or anything but I believe Fusaichi Pegasus was a June Foal as well as Fappiano - both by Mr. Prospector - it didn't seem to affect them much being end of the season breedings.