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

[Medium Rare]

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.

 

[librarian]

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

 

[librarian]

From the above paper

 

[Hopster1000]

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.

 

[Hopster1000]

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.

 

[Dale]

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? 

 

[knabe]

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.

 

[Medium Rare]

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.

 

[knabe]

here's a thick bull


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

i've seen a few sons that were thick.

 

[Hopster1000]

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?

 

[knabe]

is he naturally just thick then?

Yes. Him and sons top sellers at jlg

http://www.jlgenterprises.com/

Jlg is awesome.  Anyone wanting entry into calif dairy should contact them. They have a few odd breeds/bulls as well as mainstream angus and Holstein.

 

[Hopster1000]

is he naturally just thick then?

Yes. Him and sons top sellers at jlg

I know there is plenty of thick shorthorns as well, but sometimes it is hard to tell just what is naturally thick and what is myostatin. Would all breeds not have similar issues with single carrier myostatin sires?
I've used quite a few carriers, sometimes because I didn't realise it and sometimes because other options were not available.
Have bred a myostatin free bull that I thought was good enough and reasonably thick and I used him this year.
He's a grandson of the Australian bull Broughton Park Thunder and his dam goes back to Ballyart Vantage. He's a 2 year old.
Hope I've got the pictures right!

 

[Medium Rare]

I know there is plenty of thick shorthorns as well, but sometimes it is hard to tell just what is naturally thick and what is myostatin. Would all breeds not have similar issues with single carrier myostatin sires?
I've used quite a few carriers, sometimes because I didn't realise it and sometimes because other options were not available.
Have bred a myostatin free bull that I thought was good enough and reasonably thick and I used him this year.
He's a grandson of the Australian bull Broughton Park Thunder and his dam goes back to Ballyart Vantage. He's a 2 year old.
Hope I've got the pictures right!

Was Vantage as wide at the ground as he appeared? What was his hip and pin width like?

 

[Cabanha Santa Isabel - BR]

8)

 

[Hopster1000]

Was Vantage as wide at the ground as he appeared? What was his hip and pin width like?

I didn't see him when I was young (I would have been still in single figures myself when he was born) so just going by pictures. My cow is a grand-daughter and she is not the biggest (by our standards) but she is broad, smooth shouldered, good backed with 2 wide pin bones. Always calves herself. Has had four 36kg calves by four differently bred bulls, although she could easily calve bigger calves.
If I could get my hands on Vantage semen I would definitely use it.

 

[aj]

Interesting to me that cattle.........will have an individual that shows up that is just different. If it's different in a good way.......breeders tend to select for it. Then lines develop like TH, PHA, etc etc.. Seems like a few half brother-half sister matings should be done by breeders as just a routine.

 

[Duncraggan]

Was Vantage as wide at the ground as he appeared? What was his hip and pin width like?
[/quote]
I toured Ireland a number of years ago, probably early 2000's, to look at Shorthorns with the view to importing some genetics after hearing about the success in N. America.
I must have visited 5-10 herds, from 10 -lots of females, including the Uppermill herd in N. Ireland, and was amazed by the tremendous width and capacity of the cattle. Their size was also astounding.
I saw a Kilfrush Vantage bull that was an amazing, there were a number of them at the time and I don't recall which one I saw, son of Ballyart Vantage. He was roan, very wide over the shoulders and hips, and masculine in his build. Wedge shaped like a good mature bull should look!
I eventually settled on a bull called Deerpark Furty, after seeing some excellent progeny in the South Western part of Ireland at Limerick. Dovea Genetics would only allow me to take 50 doses as he was dead, so I took about 100 doses of Dovea Sir James 2nd as well, to make the importation economically viable.
I subsequently found out that Furty was a THC bull and slaughtered all the progeny I had as we didn't have the test available in South Africa at the time. The Sir James progeny has been mediocre, at best.
I should probably revisit these bulls as the TH test is now available. The Furty progeny was very hairy, not ideal for South African as we have heat as well as a tick challenge to contend with.

 

[knabe]

really, the only double muscling allele to mess with is the piedmontese allele.


with a homozygous animal, the tenderness is intermediate to homozygous states, unlike other alleles supposedly due to the mutation being way at the end of the gene and allowing it to have some effect in a hetero state or some other similar explanation.