Heritage/Native Shorthorn Bull Listing

[Willow Springs]

I guess it is a chicken and egg thing. Durham Shorthorns were used to create the Maine Anjou breed. Do they know if the the Durhams brought the Myo into the Maines, or if it existed in the French breed that was crossed with the Durhams? This statement from a scientific paper would seem to answer that question - "The double muscling syndrome was first documented some 200 years ago in Durham cattle by the Englishman, George Culley (1804)". Thus the reason the Durham cattle were used to create Belgian Blue and likely why the Maine Anjou cattle carry it. Hard to say that because an animal carries Myostatin it must have an incorrect pedigree.

Yes the rumours say that the pedigree is wrong, but I haven't read or heard someone say so definitively. Rumours are sometimes true and other times people just spouting off that they heard from a guy who talked to a guy.

Actually the E226X MYO mutation in Western Canadian pedigrees is believed to originate with a cow that by pedigree would qualify as Native. Pedigree link below.

https://csa.digitalbeef.com/modules.php?op=modload&name=_animal&file=_animal&search_value=&animal_registration=F624382&member_id=

The pedigree is wrong

Maybe knabe can help me here— Are there any verified examples of an exact same mutation occurring in two separate populations?

My thoughts are no.

And with that said, the only viable explanation is that the pedigree is wrong and the cow in question is in fact  a crossbred Maine Anjou.

 

[Hopster1000]

I guess it is a chicken and egg thing. Durham Shorthorns were used to create the Maine Anjou breed. Do they know if the the Durhams brought the Myo into the Maines, or if it existed in the French breed that was crossed with the Durhams? This statement from a scientific paper would seem to answer that question - "The double muscling syndrome was first documented some 200 years ago in Durham cattle by the Englishman, George Culley (1804)". Thus the reason the Durham cattle were used to create Belgian Blue and likely why the Maine Anjou cattle carry it. Hard to say that because an animal carries Myostatin it must have an incorrect pedigree.

The general consensus in the UK is that the Shorthorn always had the myostatin gene and it was more likely that Maine Anjou and Belgian Blue got the myostatin gene from the shorthorns than the other way around.
Even looking at some old black and white pictures the muscle definition on one or two bulls (that would have been native bred) would lend you to think myostatin was present. Now, as to which variant originated in the Shorthorn breed it is hard to say. Most breeds have more than one variant, as in Shorthorn. The F94L variant is most common in Limousin cattle, but they obviously have other types also.

 

[librarian]

For those interested in using Heritage Shorthorn to add rib and reduce height in your existing herd ( of any breed, but in particular "mainstream" Shorthorn).
I have just been up to DMH cattle to look at the 2019 bull calves. Ordinarily many of these calves would have gone to be developed for the Galbreath sale, but this year they remained on the farm. This group is sired by a Leader 6th son, a Catalyst 20 son and a Kodiak son. I am not exaggerating to say this group of calves had more depth and rib than whatever else is out there. Those who know how excellent the CCL6th daughters are will see the usefulness of using one of these Leader 6th grandsons back on them.
I direct those who have interest in short red bulls to Morning Glory by Titanic.
However,it was the Cat 20 grandsons that I liked best. The pictures on the DMH website and the Heritage Shorthorn site are not comprehensive or up to date and do not even begin to represent their type changing quality.
I came home with a Cat 20 grandson (Felix) and a Cat 20 granddaughter out of a Maverick daughter out of a Minn Max daughter. Four heifers are at the Iowa feed trial. This is just a heads up to you guys that this is a good year for outstanding breeding combinations if you have a Heritage influenced program.

 

[knabe]

There are regions in genome that are sensitive to mutation.

It’s not out of the question that multiple spontaneous mutations could occur in the same gene at the same spot.

Odds are probably affected by whether it’s a transition or transversion mutation.

It’s not clear yet I don’t think why different areas of the genome are susceptible to mutation from whatever like x-rays, UV, replication errors.

 

[librarian]

I also came home with a white Leader 6th grandson. This animal was longer bodied than anything else in the pen and lighter boned. None of the other L6th grandsons were built this way.  I have to admit their is something in him that makes me think of Whitehall Sultan, and my hope is that he will be an outstanding  A2 cowmaker for my Blue Grey program of Galloway crosses.

 

[knabe]

Make sure you feed him in a contemporary group and get them all scanned.

That type is one type that is a suspect for marbling.

 

[Medium Rare]

Based on what I have been reading and learning lately the F94l variant is also called the profit gene as it improves cutability without adding any calving difficulty.  So if it occurs in native Shorthorns why is it a bad thing?

It appears a Native homozygous F94L bull calf has recently been identified, so it appears to be readily available if a program is looking to add the gene to it's population.

 

[idalee]

The myostatin mutation probably came from Holland originally.  George Culley,  in his book Observations on Livestock,  published in 1786,  describes cattle imported from Holland called lyery or doubled-lyery.  They were described as follows in a quote from his book:  "it will feed to vast weight,  and though you feed it ever so long,  yet will not have one pound of fat about it, either within or without and the flesh (for it does not deserve to be called beef) is as black and coarse-grained,  as we generally suppose horse-flesh to be."    "However,  by the pains and attention of the breeders,  this useless disagreeable breed is now pretty well out of the country.  No man will buy one of this kind,  if he knows any-thing.  .  .  for people conversant with cattle very readily find them out,  from their round form all over,  particularly their buttocks,  which are turned like a black coach-horse."    This was before the publication of Coates' Herd Book in 1822 and this suggests that this gene had been severely discriminated against and mostly eliminated from the breed.  Reading early Shorthorn history books published subsequent to that date do not describe any cattle in the breed like this.  It is probable that  myostatin was already in the Maine Anjou progenitors (the Mancelle breed) in Europe before the Shorthorn  influence was introduced by the use of Durham bulls imported from England in 1839. 

 

[knabe]

So if it occurs in native Shorthorns why is it a bad thing?

like most human logic, if it came from what i support, it's good.
if it came from something i don't support, it's bad.


it's the origin of morality, religion, etc.


the appeal of the argument is that it can never be refuted and anyone who disagrees is a pagan etc.

 

[knabe]

It is probable that  myostatin was already in the Maine Anjou progenitors (the Mancelle breed) in Europe before the Shorthorn  influence was introduced by the use of Durham bulls imported from England in 1839.

maine's have at least two variants.
since maine's are 70% shorthorn by (declaration only) and 30% mancelle, who really knows where the variant came from.

at the time breeds "originated", they were a mishmash of everything they were selected based only on a couple of easily reproducible traits like color, and propensity for a production trait that was obviously selected for until we have the inbred populations we have now.

breeds essentially evolved with man's ability to travel, protect their assets, a whole host of other factors before the concept of breed associations.

really, breed associations just weeded out "bad" stuff in the beginning and humans popularlized easily identifiable hide color and other easily identifiable traits.

it's why you see holstein in maine's and anything and everything in everything.

breeds have almost lost their utility as now we are barely entering the beginning of looking past the hide.

breeds are just a way to create pyramids of resources.

 

[librarian]

I also came home with a white Leader 6th grandson. This animal was longer bodied than anything else in the pen and lighter boned. None of the other L6th grandsons were built this way.  I have to admit their is something in him that makes me think of Whitehall Sultan, and my hope is that he will be an outstanding  A2 cowmaker for my Blue Grey program of Galloway crosses.

regarding DMH Snowball....I reviewed an old post by r.n.reed that referred to the Magic Sultan Marshall cross. Maybe I am not so crazy to have a knee jerk impression of Whitehall Sultan when I look at this calf.
I will get a picture of the Leader 6th grandson and the Cat 20 grandson when I'm out this evening. Go back to page 3 to see my post about the Cat 20 grandsons I visited in Minnesota.

 

[librarian]

It is probable that  myostatin was already in the Maine Anjou progenitors (the Mancelle breed) in Europe before the Shorthorn  influence was introduced by the use of Durham bulls imported from England in 1839.

maine's have at least two variants.
since maine's are 70% shorthorn by (declaration only) and 30% mancelle, who really knows where the variant came from.

I think we should take a more holistic view of mutation and try to understand the conditions that influence mutations, duplications, insertions, deletions, translocations, etc.
Artificial selection pressure in an artificial environment (domestication and confinement) could predictably influence the regulation of signaling for the inhibition or amplification of gene expression.
Myostatin, as I understand it, is involved in homeostasis of skeletal and muscle development.
Inhibit myostatin signaling and hyper expression occurs.
Exaggerate signaling and atrophy occurs.
Nature has genetic mechanisms...hacks or mutations...adjustments...that seek to correct imbalance.
My view is that Myostatin regulation is impaired by confinement, so nature seeks to overcome loss of muscle mass  feeding by blocking Myostatin expression.
What about draught? Here we have over training of muscles beyond what is normal used in the wild.  Somehow, again reduction in Myostatin expression is being signaled. In one instance to overcome hypertrophy, in another in response to overexertion.
Add to this the modern practice of growth hormone implants.
Why would we not expect to see similar genetic solutions to regulatory challenges in the same region of the same Chromosome across breeds? Mutation is neither random nor spontaneous. Mutation is a response  to alterations in metabolic pathways due to deviations from the conditions under which the pathway evolved.
These are just thoughts, and not that well thought out. I am just trying to advocate a modern synthesis view of how genetic expression changes rather than a narrow search for a single mutated ancestor.

at the time breeds "originated", they were a mishmash of everything they were selected based only on a couple of easily reproducible traits like color, and propensity for a production trait that was obviously selected for until we have the inbred populations we have now.

breeds essentially evolved with man's ability to travel, protect their assets, a whole host of other factors before the concept of breed associations.

really, breed associations just weeded out "bad" stuff in the beginning and humans popularlized easily identifiable hide color and other easily identifiable traits.

it's why you see holstein in maine's and anything and everything in everything.

breeds have almost lost their utility as now we are barely entering the beginning of looking past the hide.

breeds are just a way to create pyramids of resources.
[/quote]

 

[knabe]

Inhibit myostatin signaling and hyper expression occurs.

this would be another mechanism independent of a causal snp.


there may be some interactive effect, but probably hard to quantify.


perhaps what is really interesting is if this mechanism is in epd's and inflating or deflating them depending upon something else we don't understand yet.

 

[knabe]

Mutation is a response  to alterations in metabolic pathways due to deviations from the conditions under which the pathway evolved.

please find a reference. if this were true, there would be a lot more mutations.


current mutations are in line with dating evolutionary branch points.


this would disturb that whole premise.

 

[beebe]

The myostatin mutation probably came from Holland originally.  George Culley,  in his book Observations on Livestock,  published in 1786,  describes cattle imported from Holland called lyery or doubled-lyery.  They were described as follows in a quote from his book:  "it will feed to vast weight,  and though you feed it ever so long,  yet will not have one pound of fat about it, either within or without and the flesh (for it does not deserve to be called beef) is as black and coarse-grained,  as we generally suppose horse-flesh to be."    "However,  by the pains and attention of the breeders,  this useless disagreeable breed is now pretty well out of the country.  No man will buy one of this kind,  if he knows any-thing.  .  .  for people conversant with cattle very readily find them out,  from their round form all over,  particularly their buttocks,  which are turned like a black coach-horse."    This was before the publication of Coates' Herd Book in 1822 and this suggests that this gene had been severely discriminated against and mostly eliminated from the breed.  Reading early Shorthorn history books published subsequent to that date do not describe any cattle in the breed like this.  It is probable that  myostatin was already in the Maine Anjou progenitors (the Mancelle breed) in Europe before the Shorthorn  influence was introduced by the use of Durham bulls imported from England in 1839.

So if I am reading between the lines correctly you are saying that the meat quality might not be very good, correct?

 

[knabe]

I don’t know if I would make that conclusion.

The double muscle breeds were bred that way for “better” meat quality.

 

[beebe]

Yes the Piedmontese pay a premium for the Myostatin gene.

 

[idalee]

In the time before 1786,  lyery or doubled-lyery cattle evidently had poor quality meat and were descriminated against.  In the 230  years since then,  there  has been selection pressure exerted to find cattle with good meat quality combined with myostatin. 

 

[knabe]

In the time before 1786,  lyery or doubled-lyery cattle evidently had poor quality meat and were descriminated against.  In the 230  years since then,  there  has been selection pressure exerted to find cattle with good meat quality combined with myostatin.

there probably is some historical evidence of this.


not many people would think to even try this.


now there is pressure to reduce the use of double muscled cattle that don't have an intermediate effect in the homozygous state like Piedmontese cattle.


in Maines in France, the test and report culard (double muscle) status.


Limousin I think may be trying to market a hetero status product.

 

[librarian]

Mutation is a response  to alterations in metabolic pathways due to deviations from the conditions under which the pathway evolved.

please find a reference. if this were true, there would be a lot more mutations.


current mutations are in line with dating evolutionary branch points.

this would disturb that whole premise.

Well, not surprisingly, my way of thinking turns out to be controversial. https://www.science-frontiers.com/sf064/sf064b07.htm
The controversy concerns directed mutation, also called adaptive mutation. But, at least others have come to similar conclusions.
Keeping in mind that I am not an academic, but rather someone more interested in asking questions than defending ideas (many wrong ideas must be considered in the pursuit of better understanding) I persist in trying to conceptualize mutation as a response to stress rather than a random error. Myostatin mutations seem to be of two sorts...deletion of information and garbling of information. Myostatin research on fish turns out to be far more interesting than in mammals because the Myostatin occurs in many kinds of tissue, not just muscle. In mammals, Myostatin also regulates the storage of brown fat in adipose cells. Brown fat is the fat that is available for instant energy...running away from preadators, for example. Is this brown fat intramuscular fat? I think so, so it's of interest to us in terms of juicy tender meat. So, the "good" Myostatin mutation may result in increased ability to form muscle and increased ability to store brown fat. This fits pretty good with my cattle bred to pull a plow all day long. I'll call that the Conan hypothesis.But, I may have it all backwards. I'm still learning about this.
https://phys.org/news/2017-05-genetic-mutation-trade-offs-parallel-evolution.html
https://elifesciences.org/articles/24669