Mandalong Super Flag

[librarian]

Angus established a Myostatin policy in 2011.
It's very possible a lot of herd Bulls, or cows are in production that were born prior to 2011, which is around when one could assume you testing became more routine in some herds.
Since you commenced testing what has been the percentage that tested positive for myostatin mutations, or that were culled for myostatin mutations prior to testing?
I disagree that getting to the root of the carrier bloodlines is a waste of time.
Super Flag and Big Mac and 69F have  generated enough income over the years to cover the cost of testing their semen to increase our awareness.
If they test clean- then great.

 

[Okotoks]

Angus established a Myostatin policy in 2011.
It's very possible a lot of herd Bulls, or cows are in production that were born prior to 2011, which is around when one could assume you testing became more routine in some herds.
Since you commenced testing what has been the percentage that tested positive for myostatin mutations, or that were culled for myostatin mutations prior to testing?
I disagree that getting to the root of the carrier bloodlines is a waste of time.
Super Flag and Big Mac and 69F have  generated enough income over the years to cover the cost of testing their semen to increase our awareness.
If they test clean- then great.

I thought an example showing a confirmed carrier of DS and TH showing up 72 times in 4 bulls free of the defect would illustrate the importance of testing one's herd bulls! These bulls are producing excellent offspring and I do not have to worry about what animals in their backgrounds was a TH or DS carrier because they are free. On the subject of testing have you actually submitted any samples yet?

 

[librarian]

My bull has been tested for TH and PHA. He is negative.
I tested him after it came to light that Clipper King of Bapton was a TH carrier. My bull has some of that breeding so I tested him
My situation is an example of a person owning a herd sire that comes from vintage semen. Genetics that have been out of circulation for many decades are now being used. again.
Super Flag embryos were for sale not so long ago, so he is not obsolete.
Your example proves only that if one knows what defect to test for, they can select against it. If one has carrier cows then testing herd sires becomes very important to avoid homozygous expression of the defect. Why not at least give folks a heads up that they may own carrier cows or bulls from years ago?

 

[jaimiediamond]

My bull has been tested for TH and PHA. He is negative.
I tested him after it came to light that Clipper King of Bapton was a TH carrier. My bull has some of that breeding so I tested him
My situation is an example of a person owning a herd sire that comes from vintage semen. Genetics that have been out of circulation for many decades are now being used. again.
Super Flag embryos were for sale not so long ago, so he is not obsolete.
Your example proves only that if one knows what defect to test for, they can select against it. If one has carrier cows then testing herd sires becomes very important to avoid homozygous expression of the defect. Why not at least give folks a heads up that they may own carrier cows or bulls from years ago?

Actually that example proves that if a carrier is in a pedigree a person should test because they could very well be clean. It also would be impossible to"select" against without testing the current stock! Earlier I mentioned we bought a bull that was clean by pedigree and yet tested positive for TH. Either way testing is necessary. We have tested several head for DS and never had a carrier but still test our herd bulls because we want to be sure not to introduce it. Speculating on what might or might not be a carrier won't help our customers so as tests become available we utilize them.

When we discuss old bulls the problem being those people who promoted them have all since dispersed.  In my case I have semen on Eionmor Ideal 69F and I watched a package sell in 2014 for $280 a straw.  Realistically speaking it would not benefit me enough as a breeder to dispose of a valuable straw of semen when I already have a testing policy in place. I also have limited vials of Super Flag who was dead before I was born, again I am further ahead to use him and test the offspring(especially since I have no reason to believe he is a carrier)  as these are genetics that once destroyed can't be reproduced.

 

[librarian]

I already indicated that Super Flag may not be the source. The source may be something that 27C, 69F, 14K and others unknown to me may have in common.
Why did this come up?
Many people crossbred with Shorthorn.
Crossbred calves from Shorthorn cows were turning up homozygpus double muscled.
This happened in Canada.
Some of the animals I am asking about were involved on the Shorthorn side.
I got in a lot of trouble asking the other breed if certain bulls were carriers. They got mad, but I had researched that breed in depth and there are limited bloodlines.
I wanted to graft a color pattern, speckled/ linebacked, from that breed onto some Galloways to reproduce Riggit Galloways. But I didn't want a myostatin mutation.
So, to heck with them if they wont own up to it....but not to heck with Shorthorns.
I crossbreed.
For me, a heterozygous myostatin mutation is a terminal trait.
The extra muscle comes at the expense of organ capacity and bone. Double muscled animals will finish at above average dressing % and the meat will be lean without much backfat. I am not interested in lean meat- that was a fad that has come and will go. Fat is nutritious, flavorful and the essential fuel for human metabolism.
Animals with high birth weight; animals that cannot tolerate heat; cannot walk and climb; will not marble- these animals are liabilities for me. So I dont want the 10% extra muscle the myostatin mutation lures us on with.
I don't want dead cows, messed up calves or weak cattle.
So, if this mutation was carried into some Shorthorn bloodlines, I want to know. Possibly its not Super Flag-  Regarding Big Mac or his dam, 69F, 27C or 14K and the Eagle bulls, even Scotty, I am curious.
But, I'm done asking questions that aren't going to get answered. Anyone with potentially impacted genetics at least enough information now to ask their own questions.

 

[mbigelow]

Earlier in the thread it was stated that there are 9 variants and that Angus have 2.  How many are in the shorthorn gene Poole is unknown so, the sires you have identified could have separate variants. With that said, I agree with Dan an Jamie testing current sires will be more beneficial since little is known.

 

[sue]

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

You may want to call or email  ASA to update his DNA information on line. The DSF did not appear when I looked . I dont know who you would contact - Jake used to do it .  Really good bull - glad I saw him person back in the day!

 

[uluru]

Thanks Sue
I tried to record the DSF & Myo free but could not make it work on the ASA site. Got frustrated and quit.  Bob

 

[librarian]

Is Myo Free displayed anywhere when the information is is sent to ASA?
I do agree that this would be sufficient information for making breeding decisions with current sires.

The historical information on bulls would just be useful for identifying potential carrier cows, especially if replacements were saved, then their daughters saved, etc.

I got enlightened about defects with my neighbor's commercial angus. He bought the best bull he could at the Trowbridge sale, a Bando 598 son or grandson, then saved daughters for years, then started saving bull calves from them until fawn calf started showing up when he used the home bred bulls. By then it was all thru his "best" cows.
The 598 son or grandson went down the road to another farm a few years later and that guy also saved daughters- but sold the bull calves to other neighbors.
All because the 598 son or grandson, bought 10 or more years ago, made such nice calves and no one knew he carried a defect when he was bought.

Luckily we had a very honest Angus breeder in the area who started getting fawn calves from similar breeding. He made an announcement to his customers and Angus was eventually forced to acknowledge the existence of the defect and 598 as a carrier. So I was able to tell my neighbor-that calf we just brought in is a fawn calf- what bulls have you been using?

Selling clean breeding stock to current customers doesn't do a lot for the little guy who can't afford to go to the big sale, but waits to buy a "used" bull or bull calf from someone who did go to the big sale a few years ago- before testing was done.
The little guy is also The Big Guy's customer and deserves to know what's going on.

 

[mbigelow]

Maybe it should be mandatory that all bulls must have DNA on submitted before they receive a registration.  Now I not sure what the cost would be but, you think we could get the cost down if that many samples were submitted annually.  This idea sounds simple but, I hate forcing people to do things. 

 

[Okotoks]

Maybe it should be mandatory that all bulls must have DNA on submitted before they receive a registration.  Now I not sure what the cost would be but, you think we could get the cost down if that many samples were submitted annually.  This idea sounds simple but, I hate forcing people to do things.

It is costing us $120.00 to test for the TH, PHA, Myo and DS! Plus a DNA profile for $45.00 , plus $25 whole herd fee. $190 is a lot so making that mandatory would drive a lot of breeders away.We are doing panels on some of them too (I don't know that I am a large breeder but I am a longtime breeder) Evidently buyers don't feel they should do the tests themselves if they are a small operation but if you are buying a proven bull for a discount the test is $30.00! :.I am not about to come on here and speculate which of the older bulls might or might not be carriers of this or that lethal or disruptive condition nor is it my responsibility to do even more tests. It's time a whole lot of breeders step and do some tests of their own!  I am hoping after a couple of years we will have verified our herd clean of all defects by pedigree and then we would just have to test our herd bulls.

 

[764wdchev]

Are you ordering the tests through the ASA? TH, PHA, and DS should be $69, but I don't see anything on their submission form for myostatin?

 

[Okotoks]

Are you ordering the tests through the ASA? TH, PHA, and DS should be $69, but I don't see
anything on their submission form for myostatin?

No we order tests through CLRC but with the exchange rate your 69 is 91 Canadian so pretty much the same thing. Myostatin is one of the options on our form.

 

[librarian]

https://shorthorn.org/genetic-condition-information-testing/

The standard tests are for TH, PHA, and DS
Myostatin testing is not even mentioned on the ASA site.
Why would some breeders routinely perform myostatin testing if there has not been an issue?
If Myostatin mutation carriers are not identified, how would one know they bought a "discounted" potential carrier and should test?
Angus is advising producers with Myostatin mutation carrier cows to outcross to a breed that does not carry the mutation- where does that leave Shorthorn in the future?

”  If buyers have problems with an Angus bull—siring calves with a genetic defect–they will buy something else.  If their commercial herd is Angus based, they are at risk for doubling up genetic defects and conditions if they use a bull that might carry the same recessive trait that might be in some of their Angus-based cows (daughters of other Angus bulls that might have been carriers).  If a rancher doesn’t know the status of a bull, it would be safer to use a different breed (one that’s not Angus-based or doesn’t carry Angus genetics); then that particular defect would not be doubled up and could not crop out in the calves."
http://angusicon.com/2013/10/genomic-testing…again

When testing does occur, even if not mandated, it would be really useful to record the tests results in WHR, in columns just like birth weight or other data. Then one can just look up an animal, go to progeny, and see how many tested positive for any given genetic condition.

 

[jaimiediamond]

We are the only breeders who came back and said hey we have a protocol in place.  We will only sell bulls that are free of all defects.I have attached a study of myostatin that refutes it originated when Shorthorns spread to Europe but instead in the Friesen breed before becoming specialized in milk. The Shorthorn variant is the same as the Maine Anjou and this would be an obvious source since Maine Anjou was accepted into both the British and American herdbook. On top of which there are several suggested sources of Maine Anjou introduction in at least 3 countries where Maine animals were introduced with a Shorthorn pedigree. These are speculation but appear to be true but there is no way of verifying these claims. So the source is Maine Anjou an unknown number of times! spec·u·la·tion ˌspekyəˈlāSH(ə)n/ noun 1. the forming of a theory or conjecture without firm evidence. Compound this with the grading up option and myostatin could have been introduced from several other breeds. There is myostatin in GALLOWAY, Angus, Hereford, Longhorns besides most European breeds. Testing of prospective bulls would be prudent! Especially when you have been suggesting that there is more Galloway influence aside from the initial introduction from Charles Colling in 1791 which was referred to as the "Alloy blood".  See quoted text below regarding myostatin. 

I am dropping this topic as for me it's no better than beating a dead horse <deadhorse>.  You suggest that a person that buys one of our bulls from a neighbor or an auction is one of our customers.  In actual fact they are the customer of the people they are buying the bull from.  In that case they can a) request a test before paying b) if purchased from auction test bull themselves or c) my personal recommendation buy from a reputable breeder and request all tests that you require to sleep soundly at night.

http://pendientedemigracion.ucm.es/info/genetvet/Myostatin-haplotype_beef_cattle.pdf

"4.4. Introducing the phenotype The pattern of haplotype sharing is an indicator of the history of the different bovine populations, or breeds, so the distribution of shared haplotypes is very useful to investigating population relationships. In the last century, different explanations on the origin of the double-muscled phenotype in different continental beef breeds were proposed. One hypothesisisthe 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]. In order to test the hypothesis of the introduction of the double muscling alleles from a single breed, we studied the relationships between the different haplotypes deduced from the complete coding sequence, using the Kimura distance (which allows to consider transitions as well as transversions) and the construction of a Neighbour Joining tree (Fig. 2). The examination of these relationships between the haplotypes showed haplotype 3 as the wild type from which all mutations have arisen in four defined groups: the first cluster was missing intronic 374–51 (haplotypes 2, 9, 7 and 20); the second cluster groups haplotypes 4, 5, 10, 13, 15 and 17 by sharing a set of intronic mutationsfound together(nt374–51, nt374–50, nt374–16 and nt414), a third group included haplotypes 1 and 11, and finally the fourth was integrated by 19, 12, 18, 14, 6, 8 and 16. Among these four groups, one set of “old” haplotypes appeared at equivalent times, that is those integrating the last group and also 1, 2 and 9, while haplotypes 7, 20, 4 and 11 arose later and more recently those haplotypes belonging to the second cluster, with 10 being the most recent (Fig. 2). Myostatin diversity in beef cattle 115 The consideration of these relationships between haplotypes should make the evolution of the myostatin gene easier to understand. The existence of many different haplotypesthat are not rooted in a common mutated ancestorseems to definitely refute a Shorthorn-Durham origin forthemuscular hypertrophy phenotype. Although there was an important introduction of individuals belonging to this breed across Europe at the end of the 19th century and at the beginning of the 20th, especially in grassland (oceanic) territories, the analysis of the myostatin gene of this breed at the present indicates the lack of any mutation. However, the theory of a founder mutation (nt821(del11)) spreading from an epicentre localised in the Friesian or Black Pied breed, much before its large specialisation into milk production seems much more congruent. There is much evidence of a hypertrophic phenotype in this population [20,38] before the organisation of the breed and selection for high milk specialisation and before the migration of this population into several milk breeds, (e.g., Normande or Parthenaise) before 1950. It is important to note that during these years, most breedsin Europe were dual purposes, and they have only recently been selected specifically for beef or milk production. This can explain the introduction of haplotype 2 from the Friesian breed to dairy (Normande), and beef breeds (Aubrac, Blanc Bleu Belge, Parthenaise, Asturiana de Valles, and Rubia Gallega), after a large diffusion of this breed before the nineteen-fifties and later. In an attempt to improve the beef characters of some breeds, the selection of individuals that were heterozygotes for the disruptive mutation may have occurred through all northern and western Europe including Spain, France, the Netherlands, Belgium, Germany and Austria. For instance, the Moyennne and Haute Belgique breed, issued from this milk purpose population, became the Blanc Bleu breed through fixation of mutation nt821(del11) and later selection for mh expression [17,18]. This phenomenon has been performed through different waves made evident when observing the large linkage disequilibrium found in Asturiana de Valles showing a more recent introduction [11]. Other breeds have been left apart from these migratory movements: this is the case for the Maine-Anjou, Charolaise and Gasconne located geographically in the French continental grasslands, in which particular mutations arose later with no spreading to the surrounding populations, or even in some cases (e.g., Limousine) have never appeared. According to this hypothesis, the results found for the British breeds were congruent since only individuals belonging to the South Devon showed a disruptive mutation corresponding to haplotype 2 which could have been introduced from exchanges with the Friesian or Black pied breed which have been highly documented in this country [20]."

 

[mbigelow]

By submitting dna, I meant just turning in the sample and storing it for a 10-15 dollar fee.  Then the owner or new owner could test easily at anytime.  I have the same thought to test all herd sires and use only those that are free until pedigree provides proof of no carriers.  I think in reality testing herd sores will pay for itself very quickly.

 

[aj]

Just to make sure......is this deal considered lethal or a non lethal defect?

 

[librarian]

Non-lethal.
Homozygous doubled muscled calves usually live, although reduced organ capacity makes them vulnerable to respiratory illness, fatigue and heat exhaustion.
Heterozygous calves are difficult to recognize.
Dystocia is a problem and carrier cows, bred to carrier bulls, producing homozygous calves will be at risk- so it can be lethal in that respect.
My own opinion about selling breeding stock is that if I discover a potential defect in anything I bred, that should be tested for, then its my responsibility to inform my customer so they know what they are breeding and selling to their customers.
But that's just me.

 

[knabe]

Maine's have two (4?) variants for double muscling.


http://www.vhlgenetics.com/Webshop/TestDetails/tabid/259/ProdID/102/Language/en-US/CatID/5/Double_Muscling__Myostatin__9_DNAvariants.aspx


this page lists them by breed
http://www.icbf.com/wp/wp-content/uploads/2014/06/Extended-Disease-Trait-Definitions.pdf
http://genomics.neogen.com/images/pdf/GGP_Bovine150K.pdf


Myostatin (Myo_T3811G_1) Myostatin YES Blonde d'Aquitaine
Myostatin C313Y, D182N Myostatin YES Brahman, other beef breeds
Myostatin E226X, E291X Myostatin YES Belgian Blue and Piedmontese
Myostatin F94L Myostatin YES Limousin
Myostatin nt419 Myostatin YES Maine Anjou
Myostatin nt821 Myostatin YES Belgian Blue, Blonde d’Aquitaine, Limousine, Parthenaise, Asturianaand Rubea Gallega
Myostatin Q204X, SC105C Myostatin YES Charolais, Limousin Double muscling.

angus has 821, f94l
maine's have 821, 419, 291, 226

i couldn't find a comprehensive list. 

http://europepmc.org/abstract/med/22063972

 

[sue]

Angus established a Myostatin policy in 2011.
It's very possible a lot of herd Bulls, or cows are in production that were born prior to 2011, which is around when one could assume you testing became more routine in some herds.
Since you commenced testing what has been the percentage that tested positive for myostatin mutations, or that were culled for myostatin mutations prior to testing?
I disagree that getting to the root of the carrier bloodlines is a waste of time.
Super Flag and Big Mac and 69F have  generated enough income over the years to cover the cost of testing their semen to increase our awareness.
If they test clean- then great.

I see the point and if I had Big Mac or super flag semen I would send the sample. When Improver was identified for his issues it was helpful to prioritize tests in the herd based on this knowledge.