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

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Author Topic: Haplotype diversity of the myostatin gene among beef cattle breeds, 2003  (Read 1757 times)

Offline 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].
'Those who do not understand the old will not understand the new'. -farmers quote

Offline librarian

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'Those who do not understand the old will not understand the new'. -farmers quote

Offline 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.
'Those who do not understand the old will not understand the new'. -farmers quote

Offline 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.
'Those who do not understand the old will not understand the new'. -farmers quote

Offline knabe

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Contact the authors.
"The generation that told us to question authority, has now become the Authority we cannot question!"

Offline 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.

Offline 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.
'Those who do not understand the old will not understand the new'. -farmers quote

Offline knabe

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do you want the mutation/s?
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Offline knabe

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https://www.ksre.k-state.edu/news/stories/2021/02/beef-tenderness-factors-that-influence-eating-quality.html

pretty clear that the driver for one characteristic is not universal in all cuts.


not sure what to think/do about this.
« Last Edit: July 10, 2021, 10:59:14 AM by knabe »
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Offline 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?

Offline knabe

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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.
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Offline 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." 

Offline 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!

Offline 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.
Im 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.
'Those who do not understand the old will not understand the new'. -farmers quote

Offline 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. Im a beef producer, and given that Aubrac- which carries the mutation, can produce some of the best beef, milk and cheese around- Im optimistic. Maybe its all about milk components and the beef components are value added. I dont 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.
'Those who do not understand the old will not understand the new'. -farmers quote

 

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