Mandalong Super Flag

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librarian

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If Igenity tests for all the variants of myostatin mutations that would be the place to send a sample. http://www.igenity.com.br
Testing Mandalong Super Flag would answer my question, Does he carry Double Muscling?

It is just my own speculation that he could be a carrier, because some bloodlines that go back to him have been said to carry the defect.

Double Muscling does occur in Shorthorns.

My opinion is that Shorthorn pedigrees should denote carrier status for this defect, just as the pedigrees now show the status of known or potential carriers of DS, PHA and TH. Transparency provides more complete information to seedstock buyers. This information is also important to breeders who may cross Shorthorn with other breeds that carry the defect.
 

Okotoks

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Cabanha Santa Isabel - BR said:
Do you wish test Mandalong Super Flag for what?
Where is possible do this test?
Maybe I can provide a dose for the test.
I paid to have Mandalong Super Flag tested for TH and PHA and he is free of both. I could see if they could run myostatin on the DNA on file but if I do that I will place bets on him being free and I will use my winnings to pay for the test. Frankly breeders should be testing their CURRENT herd bulls or bulls they are selling. Chasing the old bulls won't solve the problem, a carrier in the current gene pool should be the concern.
 

librarian

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The only way to know is to test. View This Animal's influence has him as paternal grandsire to over 4000 animals?
However, the more current bulls that could be tested might be 69F and 14K.
But if Winalot is the program in question, then has 27C been tested?
 

huntaway

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librarian said:
The only way to know is to test. View This Animal's influence has him as paternal grandsire to over 4000 animals?
However, the more current bulls that could be tested might be 69F and 14K.
But if Winalot is the program in question, then has 27C been tested?

Saying a programme in question has some negative connotations which I don't think is right. Yes an animal may or may not be passing on an issue but I don't think the programme would be in question. In that case there would be a lot of animals that trace back to these ancestors in many herds, are they programmes in question. Probably not what you meant but how it read.

 

librarian

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huntaway said:
librarian said:
The only way to know is to test. View This Animal's influence has him as paternal grandsire to over 4000 animals?
However, the more current bulls that could be tested might be 69F and 14K.
But if Winalot is the program in question, then has 27C been tested?

Saying a programme in question has some negative connotations which I don't think is right. Yes an animal may or may not be passing on an issue but I don't think the programme would be in question. In that case there would be a lot of animals that trace back to these ancestors in many herds, are they programmes in question. Probably not what you meant but how it read.
Your point is well made and my phrasing was poor. I apologize.
I was trying to indicate that, if one has reason to believe 69F, 27C or 14K carry a myostatin mutation, and Mandalong Super Flag is not a carrier, and Winalot Big Mac is not in the pedigree of 27C, then what common ancestor do all three share?
I see Winalot Commands Lady, daughter of Winalot Advertiser, and dam of both Winalot Big Mac and Winalot Captain 64N.

What is the relevance today?
I'm not aware of widespread testing for this mutation in Shorthorn and I don't see a code for it in pedigrees.
I am suggesting we be objective and include carrier status for myostatin mutations on pedigrees.

Angus registers all myostatin mutation carriers except homozygous Bulls, and flags all other carriers or potential carriers in the pedigree.


 

oakview

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Does anyone know how often double muscling occurs in Shorthorns?  I've had Shorthorns for over 50 years and never even heard of one until a few days ago.  I'm not going to argue the point about the importance of testing.  I just would like to know if anybody out there has ever had a double muscled Shorthorn calf and how often it might occur.  Maybe I should be glad I have Columbus in my tank?
 

oakview

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Evidently it doesn't occur very often since you can count the double muscled Shorthorns on the other thread on one hand. 

Darn those Canadians, anyway!  They give us cold weather, double muscled cattle.  If it wasn't for all the good hockey players, I'd have them sent to Siberia. 
 

librarian

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jaimiediamond said:
When Igenity tests for Myostatin they test for all 9 variants.  We have been testing all of our herd sires and bull calves regardless of bloodline
What year did you start routine testing for myostatin mutations?
Are females also tested? The problem usually comes up because people have carrier cows in their herds and then AI to an older bull or a carrier bull from another breed- then they get double muscled calves.
Oakview, I'm not just doing this to be obnoxious. I love shorthorns and don't like to see grow in fame as The Trainwreck Breed when it's preventable.
Zulu 3Z has exactly the kind of pedigree I would test if he was my bull.

Some Eagle Bulls have the typical sloping hindquarters and distinctive rump muscling that indicates heterozygous expression, but only testing can answer these questions.

Say we begin to gain traction with beef producers instead of show cattle breeders. If Angus producers begin to buy Shorthorn bulls or semen with an eye to saving the F1 females, we can't bring any new myostatin mutations in or we will lose all the acceptance we have gained.
 

oakview

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Zulu's been tested, before I even knew double muscling existed in Shorthorns.  Am I to shoot him?  Take him to the sale barn?  Use him like there's nothing wrong?  Quit raising cattle because whatever I might use in the future might have a genetic defect that we don't know exists today?  That's why I'm trying to get a handle on how often this defect even shows up.  Again, I haven't even heard of a double muscled Shorthorn until very, very recently and we've had them for over 50 years.  There aren't many documented cases that I'm aware of.  If it happens one in a million, then who cares.  If it happens one in four, like TH and PHA when mated, then I want no part of it.  As often as the suspected carriers have been used and show up in pedigrees, there should be all kinds of double muscled calves.  I've got to know more about the frequency and severity before I take definite action.  I don't think that's hiding my head in the sand, I just want to learn more.
 

librarian

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My interest is not in vilifying particular bloodlines. My concern is that the breeding stock world has changed since they have developed so many genetic tests for so many genetic conditions. The plethora of defects in Angus has changed the game. Failure to test is a greater economic  stigma today than the stigma of testing positive for carrier animals.
With so many variants of myostatin mutations, it important to know which ones occur most often in our breed.

 

oakview

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If the genetics cited in this thread are the culprit(s), there's a sale not too far from me that is absolutely full of potential double muscling carriers.  Can anybody answer the question of how often this occurs?  I read there are 9 mutations.  If so, let's say they are numbered 1 through 9.  If you mate carrier animals, do they each have to carry, for example, the 2 mutation or can one animal carry mutation 1 and the other mutation 8?  Has the "plethora" of defects in the Angus breed hurt them?  They may be proactive now, but they evidently went for many, many years without action if they have so many defects in so many animals.  I've got a lot more serious problems to worry about than if 1 of the 2,000 or so Shorthorns I've raised in the past 50 years might have been a double muscling carrier.  I need to know a lot more before I lose any sleep over it.  I just don't hear about it from anybody in any breed.  Is there a fullblood Limousin that wouldn't carry the double muscling gene?  Too many questions and not enough answers, yet.
 

Medium Rare

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oakview said:
Too many questions and not enough answers, yet.

I agree.

I'm left to sort rumors when it's fairly obvious other people know more than I do. TH taught me a lesson I'll never forget. With what little info I have been able to discover, I'll be sitting on my wallet and testing the home brews until the information becomes more widely available.
 

jaimiediamond

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librarian said:
jaimiediamond said:
When Igenity tests for Myostatin they test for all 9 variants.  We have been testing all of our herd sires and bull calves regardless of bloodline
What year did you start routine testing for myostatin mutations?
Are females also tested? The problem usually comes up because people have carrier cows in their herds and then AI to an older bull or a carrier bull from another breed- then they get double muscled calves.
Oakview, I'm not just doing this to be obnoxious. I love shorthorns and don't like to see grow in fame as The Trainwreck Breed when it's preventable.
Zulu 3Z has exactly the kind of pedigree I would test if he was my bull.

Some Eagle Bulls have the typical sloping hindquarters and distinctive rump muscling that indicates heterozygous expression, but only testing can answer these questions.

Say we begin to gain traction with beef producers instead of show cattle breeders. If Angus producers begin to buy Shorthorn bulls or semen with an eye to saving the F1 females, we can't bring any new myostatin mutations in or we will lose all the acceptance we have gained.

Our own herd personal protocol was established when we acquired a THF bull by pedigree and when we submitted DNA for registration (after using him) found out he was a THC!  Doesn't matter to me where the mix up was the fact was it was devastating for us as we had just finished cleaning up TH in the herd.  Of the daughters we kept (only 2) both turned out to be carriers. If we know of a defect we test for it, you don't know when mistakes have been made.  As we move forward every herd sire we purchase for use here has to be free of all known defects. No doubt other defects will turn up, some breeds have several more than the shorthorn breed. If you believe that all Angus breeders are testing their bulls for all defects you are sadly mistaken. I know of commercial breeders using angus that have had defective calves.This means we've started testing all herdsire prospects on a no tolerance for a defect basis.  We have never got a DS or PHA carrier but the only way to guarantee anything to a customer is to have tested for it.  While we are testing for defects we also DNA verify our bulls so that customers don't have to pay for it as well as registrations.

It's very simple for me.  I love the breed, my cattle, and the people I work with.  I respect my customers and want to guarantee to the best of my ability that they are happy with the product.

I won't point fingers on a public forum saying it's a Canadian problem, or Australian, New Zealand, European or even American specifically.  I will just say I own this breed and if there are known defects I will test, as a test is the only guarantee to my customers.
 

uluru

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Uluru Buster 6T has many of the bulls mentioned in this thread in his pedigree.
He is a direct son of 14K

6T has been tested and he is THF, PHAF, DSF and Myostatin Free

I like what Jaimie is doing with their bulls.

I have some vials of Manadalong Super Flag semen but have not used it yet.

Bob
 

oakview

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In regard to double muscling, I checked out a research paper entitled Double Muscling and Myostatin.  Again, since I know little if anything about it and nobody has really answered my questions, I looked them up for myself.

According to the research cited, double muscled cattle have 10% less bone, are higher in polyunsaturated fats, 11% to 5%, have significant carcass advantages compared to non double muscled cattle.  There are associated reproduction, growth, and fatigue issues, though.

Angus sired cattle with one copy of the myostatic gene had significantly increased carcass weight, muscle conformation score, and rib eye area, but it had no effect on fat traits.  Another study based on Angus sired cattle with only one copy of the gene showed greater yield, 67% to 63%, less fat trim, 15% to 18%, larger rib eye area, 85 cm2 to 73 cm2, with no difference in P8 and rib fat depths or in marbling scores.    The conclusion was that breeding programs that utilize 1 heterozygous parent can increase beef yield by 3.5% with no significant adverse effects.    Opponents argue improved carcass quality improvement (resulting from 1 copy of the myostat gene) comes at the expense of reproduction.  Research proves this false.  There are significant advantages to be gained from breeding heterozygous animals due to their increased beef yield and meat quality. 

The research says that the myostatin gene is not the only gene involved in double muscling syndrome.  Although the myostatin gene has a considerable effect, other more subtle effects are involved in the expression of the phenotype.  The same myostatin is found in Belgian Blue, Piedmoteise, and South Devon.  However, South Devon do not exhibit the physical characteristics as often or to the extent.  The reason for the variability in phenotypic expression lies in the fact that the effects of the myostatin gene appear to be influenced to a greater or lesser extent by a number of other, as yet unidentified genes.  While the defective myostatin gene has been found in a number of European beef breeds, the only British beef breed in which it occurs in any frequency is the South Devon.    This is because breeders have been selecting for additional muscling, but avoiding the extreme double-muscled phenotype.  Thus, almost by coincidence, they have selected not only for the defective myostatin gene, but also for those other modifying genes with the result that significant numbers of the breed (2/3) now carry the defective myostatin gene (with its associated advantages) but do not present the problems posed by those breeds with more extreme double muscling. 

From this research, one could conclude that one copy of the myostatin gene has several advantages.  The myostatin gene alone is not responsible for the double muscling phenotype, there are other as yet unidentified genes.  Maybe if we have suspected carriers of the myostatin gene, we should wait for more information before we kill or discard them.  If they have everything else we want, with a little extra muscling and the other positive attributes riding along with 1 myostatin gene, why throw the baby out with the bath? 

Another source said the University of Alberta had double muscled Angus in the 60's.  The likely source, according to the article, was the Fresian (Holstein).  Their language, not mine.

 

Okotoks

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librarian said:
http://sbts.une.edu.au/pdfs/Myostatin%20(RP).pdf
This pdf-Myostatin, Help or Hinder? Is brief and seems objective.

Before one can decide about the tradeoffs involved in including heterozygous individuals of any breed in beef production, one must test for the mutation. Identifying potential carriers by pedigree is just a way to target where to begin testing.
If one is concerned about testing for a genetic condition the quickest and best way to start is with one's own herd bulls. It costs $35 and is the perfect starting point.
The question on the beginnining of this thread was is "Mandalong Super Flag a mysostatin carrier?"
Well let's look at 4 bulls we have used in the last year. Let's look for Mandalong Super Flag in the first 12 generations and while we are at it let's look for Deerpark Improver because he is one of the original TH and DS carriers.
All 4 of theses herd sires are TH, DS and myostatin free.....
Diamond Lord Belmore 56B    - Deerpark Improver- 7 times  Mandalong Super Flag -17 times
Eionmor Piper 23Z                - Deerpark Improver- 13 times  Mandalong Super Flag -27 times
Herbourne B Manitoba Gus 13Z -Deerpark Improver- 18 times  Mandalong Super Flag -26 times
Diamond Braveheart 26B        -Deerpark Improver- 34 times  Mandalong Super Flag -42 times
Oakview's info was very informative, especially the origins of Myostatin in Angus. I have often wondered what the breed has inherited from the likes of Ayatollah who does carry some red holstein blood!
Anyway with testing at our fingertips speculation is really a waste of time, just test your bulls. I assure you if I was buying a bull from you, I would want genetic tests regardless of what was in the pedigree.

 
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