Was Seth Hancock Right About Overbreeding??

[xfactor fan]

Since you can insert a dead sperm in a ova, and have the resulting embryo develop into a normal term baby, the energy of the sperm may not be all that important. Researchers in Japan have done this research using beef cattle.

This is by the way what the folks who what to re-create the mamoth are going to try. Find a frozen mamoth, get a dead sperm and then use a elephant egg.

Sperm production may be different depending on the reproductive styles of the animals being studied.
Lions do it a lot per heat cycle-hundreds of times over a few days. Pandas do it once per year. Horses are somewhere in the middle.

A question for Mary, do you know where in the process the chromosomes are tagged as maternal, paternal? Could this be part of what is going on during the pause between the sperm joining the egg, and chromosomes matching up?

I'll have to admit the whole concept of chromosomes being tagged as maternal or paternal and acting differently depending on the origin, took some time to wrap my brain around.

Also I've tried to find the article about early embryo development. From memory, the human fertility researchers are finding huge amounts of activity from the mitochondria in the time between fertilization and implantation.

My guess is that the mitochondria have at least two functions. Energy production in mature cells, and keepers of the blueprints during early development.
Sort of "Hey, you third cell from the left, go over there and start making skin cells." "No, not you, fifth cell, you are going to be a liver and like it!"

Some of that "junk" DNA in the mtDNA may not be so much junk after all.

[Pan Zareta]

Heck, the TB stallion at ISU was test bred through collection. One day over 4 collections his concentration, progressive motility, and overall sperm count INCREASED. No one is saying thats normal, LoL, but it's possible.

If I'm recalling what I've read correctly, one reason for that increase you noted might be that immature sperm have more mitochondria. That might facilitate survival and motility, but could it also cause a problem post-fertilization, when successful cleavage & development of the fertilized ovum depend upon deactivation and elimination of the paternal mitochondrion? The means and timing of 'getting rid' of the paternal mito. is highly species specific, but I believe in all except some species of hamster it was gone before the 4-to-8 cell division.

[mary syers]

XFACTOR,
I've tried twice to respond to your ideas. Both times the computer refused to post my response. I think God is telling me something. Instead of my noise, why don't you explain tagging to us. Mary Syers

[Pan Zareta]

I know xfactor fan's talking about genetic imprinting, but I'd like to hear more about the tagging, too.

[mary syers]

adrienne,
Paternal mtDNA is not eliminated by any known mechanism. Its simply out competed. There are somewhere between 100,000 and a 1,000,000 maternal mitochondria in an ovum--specie specific. The sperm have less than a hundred--20 to 25 comes to mind, but my mind isn't as young as it used to be. Each mitochondria has several copies of mtDNA. When cell division begins, some mitochondria go with each divided cell. The few surviving paternal mito's go along for the ride. Mitochondria reproduce by budding. One makes two.MtDNA inside the mitochondria also splits between the two new mitochondria. As there are so many maternal mitochondria, the maternal population out produces the paternal population and the paternal mtDNA simply goes away as mitochondria wear out and are replaced. We know this because of genetically engineered mice. If you continually inbreed mice to the same mtDNA sire line, eventually using PCR, a small population of paternal mtDNA can be detected. You can't find paternal mtDNA, even in this over inbred animals without the miracle of PCR, but it is there. (PCR--is an artifical multiplication of DNA using heat, heat insensitive polymerase(TAQ) and known primers. Simple and beautiful. Anybody remember OJ's socks? That's how they did that.) Mary Syers

[Pan Zareta]

Mary, I thought it had been proven that mt in equine sperm are tagged w/ ubiquitin & that's how it's eliminated once the sperm enters the ovum, the main question left on the table being how did it escape elimination prior to then.

[mary syers]

Pan Zareta,
I hadn't read this one. Do you know where you read it?

By the way I love the mare you use as a sign in name. Mary Syers

[mary syers]

Jusst to answer my own question, I found this on PubMed:

Early degradation of paternal mitochondria in domestic pig (Sus scrofa) is prevented by selective proteasomal inhibitors lactacystin and MG132.

Sutovsky P, McCauley TC, Sutovsky M, Day BN.

There are 5 or 6 other papers on the same idea. Mary Syers

[Pan Zareta]

Pan Zareta,
I hadn't read this one. Do you know where you read it?

Differential Ubiquitination of Stallion Sperm Proteins: Possible Implications for Infertility and Reproductive Seasonality
http://www.biolreprod.org/cgi/content/full/68/2/688

Ubiquitinated Sperm Mitochondria, Selective Proteolysis, and the Regulation of Mitochondrial Inheritance in Mammalian Embryos
http://www.biolreprod.org/cgi/content/abstract/63/2/582?ijkey=e1d7e7b56431f4ded6e894906478167cb78f6afc&keytype2=tf_ipsecsha

Unfortunately only the first article is available free online in full text at this time. *Please feel free* to correct my conclusion re. ubitiquitin & equine paternal mt - this literature exceeds my level of fast & easy assimilation by quite a bit.

By the way I love the mare you use as a sign in name. Mary Syers

She was a good one, wasn't she. Her sire died (hit by lightning) and is supposedly buried not too far from our home place, and there are still traces of Trammell & Newman breedings in a few of our ranch ponies.

[mary syers]

So we have a discrepency in research. What else is new? Here are a few of the papers that show paternal mtDNA leakage. Mary Syers



Kvist L, Martens J, Nazarenko AA, Orell M. Related Articles, Links
Paternal leakage of mitochondrial DNA in the great tit (Parus major).
Mol Biol Evol. 2003 Feb;20(2):243-7.
PMID: 12598691 [PubMed - indexed for MEDLINE

Maternal inheritance of mouse mtDNA in interspecific hybrids: segregation of the leaked paternal mtDNA followed by the prevention of subsequent paternal leakage.

Shitara H, Hayashi JI, Takahama S, Kaneda H, Yonekawa H.

Paternal inheritance of mitochondrial DNA in mice see comments]

Gyllensten U, Wharton D, Josefsson A, Wilson AC

[xfactor fan]

Ok, here goes in simple english. I fought my way through the gene speak a couple of times just to make sure to understand what was going on.

Half of the chromosomes in any give horse come from the sire, the other half from the mare. She also contributes most if not all of the mtDNA in the egg.

At some point in the creation of the egg and sperm, a small section on each chromosome is tagged and identified as coming from the male or the female. Think of a bit of magnetic tape being recorded on, then erased and recorded on again.

So when the half sets of chromosomes link up in the fertilized egg, each chromosome pair is marked as coming from either the male or female.

Some functions are carried out by the genes on the male chromosome, and others by the genes on the female chromosome.

This was discovered when a mutation showed up that caused a huge rump in one ram on an Australian sheep station. The mutation at first looked like a simple dominant, all the F1 generation had big rumps.

Then it got complicated with the big rumps skipping around like crazy.

Took the researchers 20 years to figure out and document what was going on. They may have been the first folks to see this type of gene expression.

My first question when reading the original article was to wonder how on earth the chromosomes would know if they came from the sperm or the egg, and why would it make such a profound impact on gene expression.

Very non-Mendelian in action.

What wasn't clear was when this male/female markings on the chromosome happens. I'd figured it was something that happened during the reduction division process.

Hope this helps, I'll track down some of the papers if anyone is interested.



Hope this helps.

[BJ]

Ok, here goes in simple english. I fought my way through the gene speak a couple of times just to make sure to understand what was going on.

Half of the chromosomes in any give horse come from the sire, the other half from the mare. She also contributes most if not all of the mtDNA in the egg.

At some point in the creation of the egg and sperm, a small section on each chromosome is tagged and identified as coming from the male or the female. Think of a bit of magnetic tape being recorded on, then erased and recorded on again.
So when the half sets of chromosomes link up in the fertilized egg, each chromosome pair is marked as coming from either the male or female.

Some functions are carried out by the genes on the male chromosome, and others by the genes on the female chromosome.

This was discovered when a mutation showed up that caused a huge rump in one ram on an Australian sheep station. The mutation at first looked like a simple dominant, all the F1 generation had big rumps.

Then it got complicated with the big rumps skipping around like crazy.

Took the researchers 20 years to figure out and document what was going on. They may have been the first folks to see this type of gene expression.

My first question when reading the original article was to wonder how on earth the chromosomes would know if they came from the sperm or the egg, and why would it make such a profound impact on gene expression.

Very non-Mendelian in action.

What wasn't clear was when this male/female markings on the chromosome happens. I'd figured it was something that happened during the reduction division process.

Hope this helps, I'll track down some of the papers if anyone is interested.

Hope this helps.

I'm ALWAYS interested in the "plain english" versions of the scientific "stuff". Thanks so much for your explanation. Any further "plain english" interpretations you can provide, for those of us who avoided these kinds of classes like the plague , would be greatly appreciated Pictures and diagrams help too

Also...how would the above play into, or parallel, the "large heart gene" heredity theories?

BJ

[bcassidy]

xfactor--So in my genetics class we discussed sex linked gene expression (in humans--male baldness is carried by the female but expressed only in males---I think I got that correct, if I didn't somebody please correct me) but in reading your post, I get the sense that this phenom can occur on any chromosome pair not just the pair that determines the sex of the offspring. Did I get that right?

[xfactor fan]

Thanks BJ, glad to know it helped.

Sometimes I wonder if folks like the plain english version of the genetic stuff. Also there is such a wide range of knowledge in the readers of this board from vets and researchers to people with interest but not the scientific background to wade through some of the genetic papers.

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.

Is the stallion a sprinter with enough "heart" to get a long distance, or a miler?

What I find interesting is the idea that the X forms the forehand of the horse. This seems to hold true for the X factor horses, and for horses in general.

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.

[Pan Zareta]

BJ, I like learner.org's online textbook for plain English explanations. Here's a link to their entry for genetic imprinting.
http://www.learner.org/channel/courses/biology/textbook/gender/gender_6.html

It's worth noting, I think, that a significant amount of what is known about things like genetic imprinting, embryonic polarity, and inactivation of the paternal mitochondrion, has come from studying abnormalitites of mammalian embryos conceived with Assisted Reproductive Technology (ART). In this context that would not include simple "assistance" like AI. These abnormalities crop up within more complex and "interventional" in vitro ART such as Intracytoplasmic Sperm Injection (ICSI) which, crudely put, sticks the egg with a hollow needle and shoves a sperm into it ("You're GOING to be fertilized and LIKE it"). Several hitherto unknown or at least very rarely observed phenomena that are mutually exclusive with or at best counterproductive to normal develpment introduced themselves during the course of this 'end run' around the natural process, and one result is that much has been learned about previously inexplicable rare diseases and conditions.

But even the simplest form of ART (AI) is presently forbidden in the TB, much less techniques such as ICSI, therefore most of these esoteric abnormalities will be seen only very, very rarely in live foals, and I'm still hung up on the original question - does overbreeding reduce the # of sperm/vol. and the chances of getting a Super-Star sperm into the egg(?).

As far as I know, overbreeding *can*, but not necessarily *does* reduce the sperm/vol. and their motility. Those seem to be highly mediated by individual and age-related factors. I do wonder about the shuttling b/c sperm numbers are seasonal in the stallion. So how is this managed, if at all, in those that do both hemispheres? Lights? Pharmaceuticals? And what might be the side-effects of these if used, as well as the physiologic disruption to a seasonal animal from effectively never experiencing fall & winter?

In regard to the 'Super-Star' sperm question, it would seem to me this is most dependent upon the autosomal DNA being carried and therefore is primarily a random artifact of meiosis, sort of like shuffling a deck of cards and dealing a hand with 4 Aces - only with much higher odds against it. Obviously, the chances of success are increased if the '4 Aces' are 'held' by a sperm that's at optimal 'fitness' and motility, which may not always be the case if the stallion is overbred. And also obviously the chances of getting those 4 Aces are better as the number of hands dealt increases - which clearly is the philosophy of choice for some farms. Gotta get that MG1SW in the first crop or two.

What really hits home with me is BJ's point about common sense (which in the microcosm of top stallion breeding is an all too uncommon commodity). Does anyone really think that grumpy old Mr. P. would have lived to the ripe old age of 29, much less have sustained an active libido at that point, if he'd been used like FuPeg? I seriously doubt it.

PZ