Haplotype diversity of the myostatin gene among beef cattle breeds, 2003

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librarian

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I am still studying the F94L mutation. This is a “conservative” mutation, where there is a substitution of one amino acid with similar function for another. The mutation is non disruptive.
I need some common sense help on a hypothesis concerning Myostatin role in glucose metabolism and some possible lactation energy adaptation rationale for regulatory tweaking during evo-devo. This includes a broader concept of adaptive mutation as non random change, but feedback driven adjustment to energy requirements. https://www.sciencedirect.com/science/article/abs/pii/S1357272510003365

In this paper F94L is Haplotype 1.
https://www.gse-journal.org/articles/gse/pdf/2003/01/g350106.pdf
“ When observing the non-disruptive haplotypes, haplotype 1 appeared in the Aubrac, Limousine and Pirenaica breeds; the latter two breeds were sur- prisingly those in which most individual phenotypes are not explained by a disruptive mutation in the myostatin gene. This indicated a higher pheno- typic influence than expected for a conservative mutation (work currently in progress).”
“ The pattern of haplotype sharing is an indicator of the history of the different bovine populations, or breeds, so the distribution of shared haplotypes is very useful to investigating population relationships. In the last century, different explanations on the origin of the double-muscled phenotype in different contin- ental beef breeds were proposed. One hypothesis is the extensive dissemination of individuals of the Shorthorn breed used in the late 19th century to improve most western European bovine breeds which would explain the presence of the trait [10, 25], and the other being the Friesian breed [9, 20, 31] or more generally milk purpose black pied bovine populations from the Baltic plain (Hanset, pers. comm.), being responsible for spreading the mutation all over western Europe [25].”
 

librarian

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This actually is very relevant to Shorthorn Breeders because, lbs pedigree inference on carrier animals,  the F94L mutation runs in bloodlines going back to Scottshill Major Clark.
Potential carrier Tea for the Tillerman ...then Thornwood Major...Spiro...even Columbus and Clark should be F94L tested. Then we would have better information.
 

librarian

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For instance, this is a bull I own. The DNA tab will take you to testing information....if the information has been shared with the ASA. I do not know when myostatin testing became more common...often I research animals the myostatin columns are blank.
 

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Heritage Shorthorn

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Tea for the Tillerman, Clark, Spiro, and Thornwood Major have all tested negative for F94L.  I believe that the problem with F94L started about 1980 with a specific outside Shorthorn bull that was purchased.  Whether the he was all Shorthorn is open to question.  To my knowledge no Heritage Shorthorn bull born prior to 1980 has ever tested positive for F94L.  A list of all the old Shorthorn bulls that have tested negative for TH, PHA, DS, and Myostatin are listed on the Heritage Shorthorn Society website (www.heritageshorthorn.org) under "Bulls Tested Free of Genetic Defects".  Approximately 10-12 bulls will be added to that listed later this year.
 

librarian

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If the bull in question is Waukuru T Marshall, then it would be worthwhile testing the bulls behind him again, as well as  LaFraise Duke 3rd. As Sherlock Holmes said, first eliminate the impossible.
 

Dale

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We market some freezer beef, and carcass is of extra interest in our program.  This myostatin mutation is important to nearly everyone breeding cattle, including dairy, with the breeds listed in the 2nd article.  In Shorthorns there are 2 more myostatin mutations to deal with.  Every breeder needs to do a deep think about what their decisions are, for F94L and whatever other myostatin mutations their breed has.  "Ignorance is bliss" might not serve one well?  Research shows we are still learning!

Have individual breeders selecting for natural thickness accidently been adding double muscling over the decades prior to the testing that is available now?  Are some of the carrier breeds, yes an entire breed, not looking/testing?
 

knabe

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Dale said:
Have individual breeders selecting for natural thickness accidently been adding double muscling over the decades prior to the testing that is available now? 


i used to think this.  not sure now.


i started testing old maine sires.  there are only a few that were double muscle carriers.  just doing the testing to have it on record.  most i'm using are not carriers, and if they are, only using them on dna tested cows that are DM free.
 

Dale

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I am not sure either.  We owned another Weston Surprise bull, the 3rd.  His phenotype was thicker than most, plus his prominent stifle was something that attracted us to him.  He was in the ASA sire test and his progeny were not desirable in cutability (like a bull would likely be if he carried a double muscling/myostatin gene?).

We owned Weston Goliath, also with one Frosty Acres parent, maybe a relative to the Surprises.  Other breeders used Surprise bulls from Doc Nold.  It would be helpful to know where the F94L came from in Weston Surprise 14th's pedigree....  Maybe, as Nold, when asked what that bloodline was, said, "It's a surprise." 
 

Dale

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Weston Surprise 14th is NOT a carrier of F94L.  I apologize for my error.  The F94L carrier is DMH What A Surprise ET, right?

Thanks for the phone call, Joe S. and setting the record straight!
 

librarian

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To Knabe s’ question, do I want the mutations?
At this point, I am selecting for F94L because I inadvertently line bred for it through the Maid of Promise 189th cow. There was a flush of this cow and ET bulls produced from that flush from Weston Trademark 3rd, Weston Surprise 14th, Ball Dee Perfect Count, Cruachan Max Leader. Those are the ones I know of. Over a decade, I was impressed by daughters of these various bulls that I saw in different programs. I liked their roominess and moderate size. All I saw had good feet and udders and they seemed like all around practical beef brood cows that were stamped with a certain Shorthorn phenotype. So I started buying daughters, and daughters of daughters or daughters of grandsons and then a bull...stacking the 189 cow.
Finally, I saw F94L in red letters on a pedigree when I was searching progeny of my bull.
I’m not so much interested in who carries the mutation, but why.
Homozygous individuals are orders of magnitude more tender, according to one research paper, than heterozygous individuals. There is less collagen in the meat. The muscle fibers are longer and more numerous. There are two phenotypes, an “apple butt” type and a type that carries muscle far down the leg- “meat to the ankle”.
 

librarian

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Continued...
Fast twitch and slow twitch muscle, cortisol, energy storage in muscle, brown fat, heat production, on and on..all related to myostatin regulation. Myostatin is involved  a fascinating evolutionary story of RNA response to fluctuating energy demands in females. We are seeing F94L mutations in Shorthorns, I think, coming from the old Milking Shorthorn genetics in Dual Purpose Native herds today. If the genetic testing is correct on the old bulls I mentioned, then that leaves the dam of whatever outcross bull brought it in. The F94L mutation is not disruptive, it does not silence or delete the code for myostatin. The mutation substitutes one amino acid for another in the copy of the genetic code, tweaking Myostatins’ role in energy metabolism.
It remains to be seen if the meat, with less fat and collagen and with increased cutable muscle yield, is savory as well as tender. I’m a beef producer, and given that Aubrac- which carries the mutation, can produce some of the best beef, milk and cheese around- I’m optimistic. Maybe it’s all about milk components and the beef components are value added. I don’t know. Getting all sideways about who carries the gene is not my point...my point is trying to figure out the inheritance and how that history relates to custom beef production today.
 

librarian

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knabe said:
so you want animals to display double muscling?
No, not in any extreme phenotypic way. If there is some kind of metabotype advantage in terms of feed intake and bone to muscle ratio, reduction of back fat and increase in tenderness, increased disease resistance or enhanced cold weather frugal maintenance or an A2 A2 milk fat connection,I’m interested in exploring that. I don’t see the F94L variant as a negative genetic mutation, I see it as an ancient energetic flexibility that we don’t understand very well. If anything, we have probably bred a lot of that flexibility out by this or that aspect of domestication. Until it causes me a problem, I’m going to maintain the mutation in my herd..
 

librarian

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librarian said:
knabe said:
so you want animals to display double muscling?
No, not in any extreme phenotypic way. If there is some kind of metabotype advantage in terms of feed intake and bone to muscle ratio, reduction of back fat and increase in tenderness, increased disease resistance or enhanced cold weather frugal maintenance or an A2 A2 milk fat connection,I’m interested in exploring that. I don’t see the F94L variant as a negative genetic mutation, I see it as an ancient energetic flexibility that we don’t understand very well. If anything, we have probably bred a lot of that flexibility out by this or that aspect of domestication. Until it causes me a problem, I’m going to maintain the mutation in my herd..
In fact, as a test these,  I think I will carry on line breeding for homozygotes and report back later on carcass quality as well as feed intake and disease resistance.
“ Corresponding to the effects on collagen, the F94L myostatin variant genotype increased tenderness. The homozygous F94L AA variant genotype resulted in a 15.4% decrease in peak force com-pared to the wild-type homozygote (CC) (Fig. 4). This effect was seen in both aged and unaged beef. There was a significant difference in compression toughness of 9.8% between the homozygotes.Campo, Sañudo, Panea, Alberti, and Santolaria (1999) found that meat from double muscled animals in general was more tender than that from normal animals shortly after slaughter. However, this effect on tenderness disappeared after ageing for the meat for 14 days post-slaughter (Campo et al., 1999). The results herein show that the effect of F94L myostatin allele on tenderness was still significant for both peak force and compression after aging for 26day” https://www.researchgate.net/publication/51778044_Limousin_myostatin_F94L_variant_affects_semitendinosus_tenderness
 

Hopster1000

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The incidence of myostatin in the cattle isn't a major problem for me as long as I know it is there and can plan for it. However I am starting to be of the opinion that it is much better to breed cattle without it, for one main reason, and that is because I think it hides narrow cattle. Not always, but you will soon find out when you get offspring from a myostatin carrier that is free from the mutation.
Suddenly what you had thought of was a thick line of cattle turns out to be not when the myostatin mutation is bred out of it.
A single mutation doesn't seem to cause problems with milk, calving or fertility etc It's the thickness that disappears when it disappears is my issue with it.
 
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