Myostatin gene

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aj

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I guess I assume that "hot Commodity" is a carrier of some sort of the myostatin deal.
 

Okotoks

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aj said:
I guess I assume that "hot Commodity" is a carrier of some sort of the myostatin deal.
I don't think he is. The UK now requires all bull calves to be tested for myostatin before being registered. Australia now requires all imported bulls to be mystatin tested before registering them. I really don't understand why AI sires and herd bulls are not being tested by breeders. If a bull is tested it's a lot easier to make informed breeding decisions.
 

librarian

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I have been reading a lot about Myostatin. When Myostatin is inhibited from regulating muscle growth, not only the number of muscle fibers continue to increase, but the type of muscle fibers that increase are the type II fast twitch fibers. Normally the muscle fibers in cattle are predominantly type I slow twitch fibers. Fast twitch and slow twitch muscles have different metabolic pathways for burning energy. Fast twitch fibers draw quick bursts of energy ( speed and strength) from circulating blood sugar and slow twitch muscles burn stored fat. Fastvtwitch muscles are bigger and stronger, but they fatigue quickly after blood sugar is exhausted. The animals pre slaughter and the meat, post slaughter, must be handled with care to prevent the muscle from becoming dark and tough. Before death the muscle may be more tender...but that can change with stress and temperature.
Fast twitch muscle is less insulin resistant than slow twitch because instead of sugar in the blood being stored as fat, it is burned for energy. Myostatin inhibition is being studied as a treatment for diabetes for this reason.
So, when I propose that Myostatin inhibition by the various mutation in cattle is an upstream response to recalibrate the metabolism to better survive downstream stress...at least there is logic to the idea. What is the fattening process other than lack of exercise and a high calorie diet? Cattle are evolved to walk, graze, rest and flee from predators occasionally. Most of the time they just walk and graze. Change the conditions of existence and nature might respond with variations in the dosage of the proteins that gene regulatory networks produce. Some are better, some worse. Heterozygosity is generally advantageous. So, I think the question is not whether a mutation is good or bad...profitable or not, but are these mutations advantageous under the conditions your cattle are living in? Beyond that, are the animals being handled in such a way that their muscles are not exhausted at the point of death and is the meat being handled appropriately to maintain tenderness?
http://www.esalq.usp.br/lepse/imgs/conteudo_thumb/Recasting-developmental-evolution-in-terms-of-genetic-pathway-and-network-evolution-------and-the-implications-for-comparative-biology-1.pdf
"Thus, while the concepts of pathway and network evo- lution outlined in this paper are neither particularly abstract nor difficult, they constitute a challenge to traditional think- ing and experimental analyses in both evolutionary and com- parative biology. Accordingly, their incorporation into the standard thinking of these fields might well proceed slowly."
 

beebe

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So if a person had a bull that would increase the percentage of primal cuts and increase the tenderness it would seem like a person in the grass finished business where tenderness is so important would be very interested in that bull.  It seems like a bull with two copies of the F94L variant could be that bull.
 

librarian

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Yes...maybe. My opinion is it would take a lot of observation and quality control to determine if the final product was more palatable.  The producer would have to understand the physiological differences in the muscle fibers they are producing and have input on the processing protocol. Less fat cover means faster cooling. Cold shortening is an issue. The metabolic rate is higher in an animal with more fast twitch muscles and the internal temperature is higher. This affects post mortem ph. The amount of myoglobin in the blood is less and the meat could be pale or soft. Optimal slaughter age might be younger. All I really understand is that the mutation might be natures way of helping the animal dump excess blood sugar to prevent pathological obesity.
https://www.britannica.com/technology/meat-processing/Myoglobin-content
 

librarian

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Here is the ad our beloved steerplanet is showing me because I have been searching diabetes, obesity and metabolism.  The Myostatin mutation is addressing the same issue in cattle, I think.
 

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knabe

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librarian said:
Here is the ad our beloved steerplanet is showing me because I have been searching diabetes, obesity and metabolism.  The Myostatin mutation is addressing the same issue in cattle, I think.

Myostatin is involved in the pop-up ads?

And if one has the right defect, they go away?
 

librarian

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Almost. You must be thinking of Buyostatin....one of the cyber-proteins.  If you inhibit Buyostatin, pop up ads become more numerous...sometimes to the point of squeezing out all other text.
 

Dale

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CSB BAXTER LEARJET G23
Homozygous Carrier (of F94L)

His photo is on digitalbeef.
 

librarian

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librarian said:
I have been reading a lot about Myostatin. When Myostatin is inhibited from regulating muscle growth, not only the number of muscle fibers continue to increase, but the type of muscle fibers that increase are the type II fast twitch fibers. Normally the muscle fibers in cattle are predominantly type I slow twitch fibers. Fast twitch and slow twitch muscles have different metabolic pathways for burning energy. Fast twitch fibers draw quick bursts of energy ( speed and strength) from circulating blood sugar and slow twitch muscles burn stored fat. Fastvtwitch muscles are bigger and stronger, but they fatigue quickly after blood sugar is exhausted. The animals pre slaughter and the meat, post slaughter, must be handled with care to prevent the muscle from becoming dark and tough. Before death the muscle may be more tender...but that can change with stress and temperature.

Fast twitch muscle is less insulin resistant than slow twitch because instead of sugar in the blood being stored as fat, it is burned for energy. Myostatin inhibition is being studied as a treatment for diabetes for this reason.
So, when I propose that Myostatin inhibition by the various mutation in cattle is an upstream response to recalibrate the metabolism to better survive downstream stress...at least there is logic to the idea. What is the fattening process other than lack of exercise and a high calorie diet? Cattle are evolved to walk, graze, rest and flee from predators occasionally. Most of the time they just walk and graze. Change the conditions of existence and nature might respond with variations in the dosage of the proteins that gene regulatory networks produce. Some are better, some worse. Heterozygosity is generally advantageous. So, I think the question is not whether a mutation is good or bad...profitable or not, but are these mutations advantageous under the conditions your cattle are living in? Beyond that, are the animals being handled in such a way that their muscles are not exhausted at the point of death and is the meat being handled appropriately to maintain tenderness?
http://www.esalq.usp.br/lepse/imgs/conteudo_thumb/Recasting-developmental-evolution-in-terms-of-genetic-pathway-and-network-evolution-------and-the-implications-for-comparative-biology-1.pdf
"Thus, while the concepts of pathway and network evo- lution outlined in this paper are neither particularly abstract nor difficult, they constitute a challenge to traditional think- ing and experimental analyses in both evolutionary and com- parative biology. Accordingly, their incorporation into the standard thinking of these fields might well proceed slowly."
A very straightforward review of the pros and cons of Myostatin mutations in beef production
http://www.beefmastersa.co.za/images/photos/46-78-Beefmaster_Journal_2019.pdf

 

librarian

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Haplotype diversity of the myostatin gene among beef cattle breeds
Susana Dunner, M. Eugenia Miranda, Yves Amigues, Javier Can ̃ ́on, Michel Georges, Roger Hanset, John Williams, Fran ̧cois M ́enissier
https://www.researchgate.net/publication/281501888_Haplotype_diversity_of_the_myostatin_gene_among_beef_breeds/fulltext/55f8d82c08ae07629de131d0/281501888_Haplotype_diversity_of_the_myostatin_gene_among_beef_breeds.pdf?origin=publication_detail
"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]."
 

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knabe

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A market for less beef but of better eating quality and with environmental credentials and provenance will potentially lend itself more to forage based systems and inputs perceived as more ‘natural’. The Beef Shorthorn is well placed to position itself as a breed that does all of this and more. However, a careful eye on sensibly exploiting the Myostatin deletions for the current market while conserving the breed’s other attributes may serve dividends in keeping the Beef Shorthorn relevant to future markets."

article is misleading.

any breed has the same capability of shorthorns with regard to the myostatin gene. really, the only breed that is well placed is piedmontese. they seem to have two types of homozygous lines.  one's that appear normal, and ones that appear heavier muscled.

normally, the breed is homozygus.  However, recently a bull was found to be heterozygous and a notice went out within the breed.

almost every breed has the same literature. there is simply more diversity within than between breeds.
 

Medium Rare

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aj said:
So on Learjet......could he be a carrier on both sides?

If he is out of who his pedigree says he is, they are both carriers. There's also the possibility that they are more than carriers.
 
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