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 3807 times)

Offline knabe

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so you want animals to display double muscling?
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Offline librarian

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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,Im interested in exploring that. I dont see the F94L variant as a negative genetic mutation, I see it as an ancient energetic flexibility that we dont 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, Im going to maintain the mutation in my herd..
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Offline librarian

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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,Im interested in exploring that. I dont see the F94L variant as a negative genetic mutation, I see it as an ancient energetic flexibility that we dont 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, Im 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, Saudo, 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
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Offline 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.

Offline knabe

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 but you will soon find out when you get offspring from a myostatin carrier that is free from the mutation.



interesting observation
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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.

I think most people over look this.

Not only is it a false phenotype, but it is also affecting the numbers. The system can't comprehend that the marbling and rib eye are unusual for a reason or that the ww an yw might out perform the prediction. Throw a half a dozen carriers into the breed organized sire test and you have a mess within what was already a borderline statistical guess.

I plan to use a well known e226x carrier on a myo free cow, for non muscling reasons, and have found an F94L carrier I would also like to try. The F94L carrier's phenotype is the reason I was interested in using him, but his test results have put him on the back burner until I convince myself there isn't a clean bull out there built like he is to try instead.

Offline librarian

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 but you will soon find out when you get offspring from a myostatin carrier that is free from the mutation.



interesting observation

This is a great observation, especially when compounded with amount of energy available for rumen fermentation.
Even though the outcome is different, there are similarities in dairy and beef cattle from a nutrigenomic perspective. For instance, both the synthesis of milk fat in dairy cows and the synthesis of intramuscular fat in beef steers are regulated by a similar network of TF. Nutrients or stimulus received with the diet (PUFAs, insulin, etc.), activates PPARα in the liver of the dairy cow and PPARγ in the intramuscular preadipocyte of a beef steer. The activated PPARs form a heterodimer with retinoic X receptor alpha (RXRA), leading to the upregulation of their lipogenesis-related target genes (Figure 2). Furthermore, in the same way, the activation of the PI3K/Akt/mTOR signaling pathway will lead to the synthesis of milk protein in dairy cows [120], the activation of the same metabolic pathway might lead to muscle hypertrophy in beef cattle, but this is a concept that has not been completely elucidated [121]. It is also worth to mention the importance of fatty acid binding proteins (FABPs) in ruminants, which bind and transport LCFA. FABP4 affects milk yield and milk protein content, both economically important traits in the dairy industry [122], and FABP4 also presents gene polymorphisms that have been associated with meat quality traits in beef cattle [123]. https://www.intechopen.com/books/gene-expression-and-control/gene-regulation-in-ruminants-a-nutritional-perspective
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Offline librarian

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

Offline 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.

I think most people over look this.

Not only is it a false phenotype, but it is also affecting the numbers. The system can't comprehend that the marbling and rib eye are unusual for a reason or that the ww an yw might out perform the prediction. Throw a half a dozen carriers into the breed organized sire test and you have a mess within what was already a borderline statistical guess.

I plan to use a well known e226x carrier on a myo free cow, for non muscling reasons, and have found an F94L carrier I would also like to try. The F94L carrier's phenotype is the reason I was interested in using him, but his test results have put him on the back burner until I convince myself there isn't a clean bull out there built like he is to try instead.

I think the single copy of myostatin in the shorthorn breed is like a false economy. The double copy (usually e226x) causes too many problems. In the UK and Ireland the F94L mutation is often called the profit gene as a double copy doesn't really affect calving or milk production.

In a perfect world the numbers should only really be drawn from non carrier cattle I think.

I have semen and embryos that have carriers of myostatin and I'm unsure whether to continue to use them or not as I don't know how thick and how much ribe eye etc a non carrier will have. For instance, maybe someone here could tell me, what are non carriers bred from Northern Legend like?

If, like you, I was to use a carrier, I would be looking to see if there was non carrier offspring that I could see.

Offline Hopster1000

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 but you will soon find out when you get offspring from a myostatin carrier that is free from the mutation.



interesting observation

E226X seems to be the worst variant for covering up inadequate base thickness in cattle. However, different breeding lines have different results when the myostatin drops out. Alta Cedar Perfect Storm lines don't seem to suffer as much. Diamond Captain Mark and Waukaru Patent lines can be hit and miss but I think the worst are the Trump lines. Good looking cattle with myostatin mutation, but completely different without it.

I should point out that is my own personal observation from a small number of cattle and when observed over a larger population it may be very different.

Even F94L isn't good when it drops out. Must LIM cattle over here have 2 copies. Which means if used on dairy cattle or beef cattle one copy will always be passed on. I have seen LIM offspring from Holstein dairy cows from a bull LIM bull that only carried one copy. The non carrier calves just looked like black Holsteins. No thickness whatsoever passed on.

Offline Dale

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Hopster1000, that is food for thought, as an old farmer used to say to the preacher on Sunday after the sermon.  Yours and other posters sure got my attention about the phenotype of offspring of myostatin carriers. 

Many hog breeds added thickness to their hams and general muscularity by infusing Pietrain genetics, a quick fix.  If one is patient, is adding natural thickness to beef cattle by selection not preferable to getting there rapidly via myostatin carriers? 

Offline knabe

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is adding natural thickness to beef cattle by selection not preferable to getting there rapidly via myostatin carriers?


it would probably be interesting to do more investigation of the poor cattle and why they are what they are as well as the "good" ones.


genetically, they are equally interesting.
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Hopster1000, that is food for thought, as an old farmer used to say to the preacher on Sunday after the sermon.  Yours and other posters sure got my attention about the phenotype of offspring of myostatin carriers. 

Many hog breeds added thickness to their hams and general muscularity by infusing Pietrain genetics, a quick fix.  If one is patient, is adding natural thickness to beef cattle by selection not preferable to getting there rapidly via myostatin carriers?

I watched several pigs die as a result of it as well. 30 plus years later, maybe even 100+ in some cases, and they're still sorting the resulting stress gene out of the populations. Some of those populations were never even supposed to have had the source of that gene in them. Odd how that works.

We made some really lean protein, that occasionally tasted funny, as fast as we could though.

Offline knabe

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here's a thick bull


https://www.youtube.com/watch?v=Gv5rL0WRwKo

i've seen a few sons that were thick.
« Last Edit: July 25, 2021, 02:10:58 PM by knabe »
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Offline Hopster1000

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here's a thick bull


https://www.youtube.com/watch?v=Gv5rL0WRwKo

i've seen a few sons that were thick.


Good bull obviously. He definitely made good money!
Does he carry a myostatin mutation?
I looked up his registration and unless I'm reading it wrong his defects are AMF-CAF-D2F-DDF-M1F-NHF-OHF-OSF-RDF. Does this bull have this many? I am still doubting that I am reading the registration page wrongly.
I could hardly believe how long the list of possible genetic mutations there are in Angus.
The list code for myostatin seems to be DM?

If he is not a myostatin carrier is he naturally thick then? And he passes that thickness to his offspring. If he were to be used on a myostatin female carrier and she passed it on, would the resulting calves then be much thicker than that sire would normally breed?
« Last Edit: July 25, 2021, 08:05:11 PM by Hopster1000 »

 

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