Myostatin gene

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GM

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Okotoks said:
mark tenenbaum said:
What about your cows? Do you think there may be comparable traits? Myostaten doesnt appear to have been on the radar (in terms of testing- sale annonucements) very long. The only reason I brought this up in your case is it seemed like a freak deal of sorts-You always seemed to go for functional cattle with non-off the wall traits-maybe there"s something in the woodpile that nobody would have been aware of a few years ago But in my ever so humble opinion: THERE IS NO REASON to dismiss or to dispose of good cattle Or" who struck John?" knowingly or not. Some of  the Canadian cattle per example are way good-Just breed em clean if they work for you O0
Myostatin is real and it needs management! It takes a carrier bull to follow a carrier bulls daughters to find that out. (Typically it just drifts along in a herd until you bring in that second bull. A neighbor of ours bought a small herd with some very good cows in it. The last year the young cows had been bred back to their half brother(their sire was a purchased bull and was a great bull with great all round EPD's, actual weights and eye appealing moderate offspring) Long story short three difficult vet assisted deliveries, one dead calf. He bought a myostatin free bull and this year the problem was solved. At our annual Alberta meeting this year a breeder stood up and said he had believed exactly what Xbar states above but after this calf crop using a carrier on carriers he said the myostatin test was cheap and the issue real!  It's all about getting the information and managing it. You can use carriers but in my experience using them back on carrier cows is an expensive mistake. It's not just a Shorthorn problem, it exists in several breeds.
The E226X was introduced to Shorthorns from Maine Anjou crosses, some legit , some not. In Canada almost all the carriers trace to a cow that produced two maternal brothers born in 1980 and 1981. The main impact from those two brothers comes from 3 grandsons of the one born in 1993,1996 and 2000 and 1 grandson of the other bull born in 1993. So its late 1990's/2000 that it really starting to be distributed through the breed by those very popular and widely used bulls or their descendants.
Who was the cow and two maternal brothers you referenced?
 

RyanChandler

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“Started being distributed in the mid 90s”

So 25 years later it was decided there was a problem?

Both of the biggest herds in Western Canada have line bred extensively to these carriers.

Is it really being implied that these folks pulled a George Ahlschwede and just kept quiet about the genetic defect train wrecks occurring within their herds over the past two decades?
 

Okotoks

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-XBAR- said:
“Started being distributed in the mid 90s”

So 25 years later it was decided there was a problem?

Both of the biggest herds in Western Canada have line bred extensively to these carriers.

Is it really being implied that these folks pulled a George Ahlschwede and just kept quiet about the genetic defect train wrecks occurring within their herds over the past two decades?
It takes awhile to spread throughout a herd and only half the offspring are carriers. If you use a non carrier relative back on the carriers you are going to get unaffected calves and only 25% will be carriers. What is 25 years 3 to 5 generations? If you started with a free herd there is no way you would see anything in the first generation and if you had a big bull battery with free sires you may not see it for 3 or 4. I'm not implying anything, does everything have to be a conspiracy these days. Genetic defects take time to spread and non lethal ones that are not always expressed the same take longer to identify. In any case there is a simple inexpensive test so breeders have that option if they choose to use it.
 

mark tenenbaum

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The simple tests are important-along with having an idea which lines may be infected or have the propensity to become a carrier when exposed to a carrier-Very basic stuff.So somebody say which cattle they suspect or have had experience with-Dont be coy boys O0
 

beebe

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One of the reasons that I brought this up is that I have an opportunity to raise Piedmontese calves for a guy at a nice premium.  I am wondering if I would be getting myself into something I might regret, particularly calving.
 

RyanChandler

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Buster 14k born in 2000 =>24M in 2002 => Saskvalley Ramrod 2005. Idk about the latters status but when the last of the grandsons born in 2000 is in many cases 10+  generations in that 25 year span.  Dozens of pedigrees where carriers have been stacked literally 5 and six times in the past 3-4 generations. 

No one implied a conspiracy. But if the prevalence of myostatin starts to surface to any real extent outside western Canada, then clearly this becomes a transparency issue with these breeders who HAD TO HAVE HAD MANY homozygous carriers, just based on the sheer number of times these genetics have been compounded within their herds.
 

Okotoks

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-XBAR- said:
Buster 14k born in 2000 =>24M in 2002 => Saskvalley Ramrod 2005. Idk about the latters status but when the last of the grandsons born in 2000 is in many cases 10+  generations in that 25 year span.  Dozens of pedigrees where carriers have been stacked literally 5 and six times in the past 3-4 generations. 

No one implied a conspiracy. But if the prevalence of myostatin starts to surface to any real extent outside western Canada, then clearly this becomes a transparency issue with these breeders who HAD TO HAVE HAD MANY homozygous carriers, just based on the sheer number of times these genetics have been compounded within their herds.
Ramrod never had a significant number of calves hit the ground until 2008, so the first offspring were not producing until 2009, 2010 and they sure were not half sibling matings. Couple the free offspring with the out cross bloodlines being used and it takes time to get to a significant number of carriers. Some double muscled calves are born fine especially out of mature cows so the issues take time to surface and a lot of people don't believe it's a problem or recognize the problem even when it happens. A significant number of breeders are testing their sale bulls in Canada, I guess it's up to the buyers to decide what they want. As of  Friday July 19, 2019 it's now mandatory to test bulls in Australia and donor cows for myostatin. The British Association is making testing mandatory as well. The article put out by the American Association seemed to down play the the importance. Some people claim it's a plus.
 

aj

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I wonder about Muridale Raw Hide 6e's status. He looks like one hell of a bull by his picture.
 

aj

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I wonder out loud about the popular AI crossbred bulls used in the club calf industry? Could the mutation be floating around out there.
 

Medium Rare

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aj said:
I wonder about Muridale Raw Hide 6e's status. He looks like one hell of a bull by his picture.

He was listed as clean on their sale sheet. I believe they've been testing their sale bulls for a few years now.
 

Medium Rare

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I went back and read the article in the Shorthorn Country. It claimed they had only tested 11 head. I know how many I've tested, which means there can't be many breeders testing for it in the states or they're not using the ASA to do the testing.

I assume I have a couple carrier cows in my herd based on a calf each has thrown and one calf I know was carrying, so all future herd bulls will have to be tested clean here. It's not an option, and any breeder wanting to sell me a bull will need to show me some results or I'll move on. The defect won't get the chance to cost me any more money. I purchased these cows, which leads me back to that 11 head tested number being even more interesting. On the other side, I recently sold a bull and out of the blue mentioned he had tested clean and the breeder obviously knew what I was talking about.

You can track one of the sources of the gene back over 50 years. When you speak with the right circle of old breeders who knew the source, it doesn't seem to have been a secret even back then. If you mention having semen on a son the response is, "ya, don't line breed to him". Some of the bulls between then and now sired relatively very few calves, but obviously it managed to hang in there until today. It appears to me Shorthorn breeders went after muscling, and they found it.

The past really doesn't matter to me as we have a test to move forward with, but if you connect the dots and read between a line or two I can't help but wonder if the source I tracked to is the same source north of the border that was used under a different name.
 

Duncraggan

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Do the AI companies test for all of this? I have brought in numerous sires to South Africa from Semex over the last 15-20 years! None are listed for TH or PHA but one is a probable DS and they all have no tests listed for Myostatin. I am getting nervous here!
Are they obliged to have the bulls tested?
 

mark tenenbaum

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I only have 3 straws on G-9-But a bunch of 2975-I dont know about Myostain-At least the BWS didnt get too crazy till the Mark 4s got mixed with Enticer-Along with growth patterns that sometines didnt make sense. However-Before TH was an issue or even known about- we used RFC Magnum-A CF Fortune out of  a picture Perfect going back to Mark 4. Lawrence had never seen nightmare trainwrecks like that. So I asked him what do the cows go back to?-Answer MARK 4. That leads me to believe with 20 plus years hindsight that  Mark 4 was TH  because the lethal  occurrences were so numerous. Id like to bust a straw of 2975-If I had the Mark 4 semen which I dont-Im wondering if 2975 would even have been Mark 4s sire in the first place-According to a number of people who would know-G-9 was thought to be a Cunia son or grandson.Which would be great with me. Im just not sure if other than maybe Hallmark how many direct sons or daughters of mark 4 or even G-9 were available in Canada O0
 

redcows

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When there were 11 tested, 3 were mine and fortunately all clean.
 

GM

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Buster 14k was mentioned and so was Ramrod.  What is the suspected starting point in Canada?  Or at least in your heard?
 

redcows

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I have heard Buster's sire, Eionmor Ideal 69F was a carrier. If so, it's likely further back than that. He does have a common sire on both sides of the pedigree, but it could have come from any ancestor.
 

aj

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Seems like when we go with an animal that is more extreme........or a tad bit different looking.......sometimes it's because of a mutation.
 

Okotoks

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aj said:
What was g9's registration number....or 2975
MILL BROOK RANSOM G 9 3550480

https://shorthorn.digitalbeef.com/modules.php?op=modload&name=_animal&file=_animal&search_value=&animal_registration=3550480&member_id=

MILL BROOK RANSOM G NINE 2975  3641922

https://shorthorn.digitalbeef.com/modules.php?op=modload&name=_animal&file=_animal&search_value=&animal_registration=3641922&member_id=


 
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