New MTDNA study on Thoroughbreds

Understanding pedigrees, inbreeding, dosage, etc.

Moderators: Roguelet, hpkingjr, WaveMaster, Lucy

stancaris
Restricted Stakes Winner
Posts: 763
Joined: Thu Sep 16, 2004 11:24 am

return the stallion to the dam

Postby stancaris » Thu Jul 26, 2012 6:50 pm

X Factor Fan: Your statement the old pattern, " return the stallion to the best blood of the dam" also might be construed as a means of increasing the chances of inheriting a superior X chromosome from these great dams. Since you are an X Factor Fan, perhaps this is some food for thought.

xfactor fan
Breeder's Cup Winner
Posts: 2212
Joined: Thu Sep 16, 2004 8:46 pm

Postby xfactor fan » Thu Jul 26, 2012 10:05 pm

Stan,
Yes it might. However, there will be some recombination down the generations, even with a stallion being bred back to his own dam. And while this might be part of the observed effect, my feeling is that it is more likely to be the mtDNA which would be identical.

Good observation. If there is an interaction between some genes and how the mtDNA expresses itself, then the observed effect might be magnified by the interaction between genes and mtDNA.

The advances in genetics is amazing. It wasn't all that long ago that Palomino breeders were culling those "albino" horses. And making a big deal out of dark skinned palominos and "pumpkin skin" palominos. Not realizing that they were dealing two different genes (Cream, and Champaign) and single dilutes and double dilutes.

A similar sea change is going on currently with the genetic research into the Appaloosa coat pattern, with the old guard defending their notions of how the coat colors are produced. Haven't seen much from them since the genetic research team found the LP gene, and have a test for it. If you are interested there are several long threads over in the allbreed forum in the research section. You may find it amusing.

(To those who don't follow this stuff, the research team at The Appaloosa Project had the theory that there were two different genes required to produce the appaloosa coat pattern. LP, which creates the typical roaning pattern, and a second gene that is responsible for the blanket pattern. Which can be just over the rump, or nose to tail spots. A horse needs both to have the classic Appy pattern. Just LP is a roan, just the pattern gene is a solid horse. They interact like the black coat color and Agouti do to produce a bay.)

stancaris
Restricted Stakes Winner
Posts: 763
Joined: Thu Sep 16, 2004 11:24 am

errors in mt-DNA

Postby stancaris » Fri Jul 27, 2012 3:23 am

X FactorFan: Here is an idea that could be important: Sometimes a sire passes on mt-DNA (rarely but it does happen). Could this be the reason why some horses carry mt-DNA that is different from what they are supposed to be carrying from their tail female line. Is it possible that the Hill study which showed errors in the stud book could be related to stallions occasionally transmitting mt-DNA?.

Another idea: Could a stallion that passes on mt-DNA be at an advantage over other stallions that never pass on mt-DNA?

User avatar
diomed
Grade III Winner
Posts: 1142
Joined: Mon Oct 04, 2004 4:16 pm

Postby diomed » Fri Jul 27, 2012 6:49 am

I don't think it's possible for a male of any species to pass on mtDNA.

xfactor fan
Breeder's Cup Winner
Posts: 2212
Joined: Thu Sep 16, 2004 8:46 pm

Postby xfactor fan » Fri Jul 27, 2012 7:18 am

Stancaris

My understanding--haven't looked at the subject in a while so this may be out of date-- is this.

When the sperm gets through the outer membrane of the egg, it delivers the chromosomes plus the mtDNA that powers the tail.
The chromosomes match up and do their thing in the nucleus of the cell, and mitochondria from the sperm tail join the rest of the mitochondria out side the nucleus in the cell cytoplasm. When a cell divides the cytoplasm also divides each new cell gets their share of mitochondria.

If you think of the cell as a fried egg, the yoke has the chromosomes, and the white is where the mitochondria hangs out. Then throw one peppercorn into the egg white. This represents the mitochondria donated by the sperm.
The next step is to divide the fired egg into four parts. The peppercorn will be in only one segment.

If the peppercorn is in a section that (now think horse embryo rather than fried egg) will become a hoof, then that cell line will have a small amount of mitochondria from the sire but will not pass this on. IF and only if the peppercorn end up in a cell line that become germ cells will the sire's mitochondria be reproduced.

Again it is my understanding that if the mitochondria is very lucky over time a cell will have two distinct types of mitochondria. A large population of maternally donated mitochondria with a much smaller secondary population of different mitochondria.

The Hill study found completely different mtDNA types in many families, they also found some "Novo" or new variations in existing cell lines, where they seem to be identified as a sub-set of an existing line.

Whether the sire's mitochondria reproduces seem to be a matter of being in the right place at the right time, rather than any special qualities of the sire. Or his genetic worth.

DDT
Breeder's Cup Winner
Posts: 2021
Joined: Tue Jan 08, 2008 1:35 pm
Location: New Jersey

Postby DDT » Fri Jul 27, 2012 7:19 am

Stan

As I understand the process, mtDNA carried by or on the sperm cell from the stallion is located on the tail or near the tail and is almost always lost during the process. If by chance that mtDNA makes it into the cell, the dam's mtDNA always rules and is passed on to the foal. If this were not true mtDNA could not be used to trace the female line.

DDT

xfactor fan
Breeder's Cup Winner
Posts: 2212
Joined: Thu Sep 16, 2004 8:46 pm

Postby xfactor fan » Fri Jul 27, 2012 11:58 am

DDT,

As I understand it that is usually the case. It is very rare that the male mitochondria get established. But as stancaris points out it does happen.

Shows up as different sized peaks in human testing.

User avatar
Pan Zareta
Breeder's Cup Winner
Posts: 2074
Joined: Wed Dec 22, 2004 10:55 am
Location: west TX boonies

Postby Pan Zareta » Fri Jul 27, 2012 12:14 pm

Persistent paternal mitochondria is indeed very rare. It is also frequently associated with pathology. Transmission of paternal mtDNA by a reproductively viable female is even more rare than simple persistence of paternal mitochondria, so rare that an argument that paternally transmitted mtDNA is as likely as error in the stud book record to be responsible for different mtDNA haplotypes within the same TB female family has no scientific credibility whatsoever.

xfactor fan
Breeder's Cup Winner
Posts: 2212
Joined: Thu Sep 16, 2004 8:46 pm

Postby xfactor fan » Fri Jul 27, 2012 2:43 pm

Ok,

Then what were the "de novo" mutations within female families that Hill documented?

User avatar
Pan Zareta
Breeder's Cup Winner
Posts: 2074
Joined: Wed Dec 22, 2004 10:55 am
Location: west TX boonies

Postby Pan Zareta » Fri Jul 27, 2012 3:07 pm

xfactor fan wrote:Ok,

Then what were the "de novo" mutations within female families that Hill documented?


Simple spontaneous mutations. Mitochondria are present in multiple copy in most cells, the actual number depending upon the metabolic activity of the cell. They replicate independently of the cell itself. Spontaneous mutations, errors during replication, are not unusual. Those that occur in d-loop are more likely to persist than those in the coding region. They only persist into the next generation if they're present in the mitochondria of the oocyte.