Heritage/Native Shorthorn Bull Listing

[knabe]

without diversity and a slow mutation rate, the ability to respond to environment is muted.


angus is bottlenecking it's population, the breed association knows it.


it's up to other breeds to preserve diversity, leverage it, and preserve it.


almost no breed has done this.

 

[knabe]

the number of muscle cells is not increased, only their size.

 

[librarian]

Brown fat is pretty confusing. It seems different from intramuscular fat. Myostatin is also involved in insulin sensitivity. http://www.oncotarget.com/index.php?journal=oncotarget&page=article&op=view&path%5B%5D=16822&path%5B%5D=53810

 

[librarian]

This is pretty interesting about breed differences in Brown Adipose Tissue in newborn calves and cold tolerance. Protein intake and cold exposure of the dam influences this. The brown fat produces non-shivering heat.
“We know calves born to cows that have gone through cold stress are usually a little bigger when they’re born. Other research has shown those calves and lambs that are born to dams that have been cold stressed posses more brown adipose tissue, or brown fat. It’s a way for those calves and lambs to adapt in utero,” explains Carstens.
The article comparing Angus and Brahman calves found that Brahman calves had higher mortality rates, especially as the temperature dropped.
“Angus calves exhibit approximately 25 percent higher peak metabolic rates than Brahman calves, which may contribute to their greater cold tolerance. It was our hypothesis that reduced BAT thermogenesis in Brahman calves may be caused by limited BAT ontogenic development during the third trimester,” states the article.
Researchers also found that Angus calves had 60 percent more cells per gram of BAT, which consequently had 60 percent more adipocytes.   
Breed selection, nutrition and supplementation are all important factors that can be used to reduce cold stress and mortality and potentially increase BAT levels in newborns. As spring storms sweep across parts of the state, calf survival in cold temperatures is an important concern to many producers.
https://wylr.net/the-roundup/archives/239-livestock/cattle/2259-brown-adipose-tissue-increases-heat-production-in-newborn-calves-and-lambs

 

[knabe]

https://nutritionrestored.com/blog-forum/topic/less-poison-vitamin-a-in-cattle-more-brown-fat-the-good-bodyfat/

 

[knabe]

would be interesting story of who figured this out 200+ years ago.

 

[Cabanha Santa Isabel - BR]

In my understanding, double muscle is part of west european cattle population.
Possibly was introduced on Shorthorn cattle through cattle from The Netherlands region on the breed formation on XVII century.
If Maine Anjou, Belgina Blue and other doube muscle breeds got their genes from Shorthorn or not will to be a question to be answered through adequate genetics tests.
By the way this population on west europe has this genes as many breeds without Shorthorn genes also show DM and cullard type as Parthenais, Aubrac, Asturiana de los Valles.
Bred and use the genetics that is useful for you. But, have in mind that the action always came with reactions.

 

[librarian]

Here is a very good summary of Myostatin considerations from the Beef Shorthorn Society in the U.K.
https://www.beefshorthorn.org/beef-shorthorn-news/2001/myostatin-and-its-use-in-beef-shorthorn-breeding

It is a follow up on this article.
https://www.beefshorthorn.org/beef-shorthorn-news/2018/11/13/double-muscling-myostatin-and-the-beef-shorthorn

 

[Cabanha Santa Isabel - BR]

Thanks Librarian. Good articles.

Point 1 - "... This is not a surprise given that the first documented case of double muscling was 200 years ago in Durham cattle." ---- So, DM is credited to be inserted in the Shorthorn population, but seeing old pics, and I saw thousands, never saw a DM animal. Maybe Dm was in so little level on the population that was expressed very few animals expressed it in decades. And, the recent widespread appearance is cause by the Maine Anjou influx that increased the genes of Dm frequency in the population, as two variants are shared by both breeds.

Point 2 - nt821 is shared by Angus, Limousin, South Devon, BB and Blondies. Interesting as Angus have not "official" influx or was introduced on that breeds.

 

[RyanChandler]

None of the defects the American Angus Association recognizes have been found in the Lowline Angus population- as all their foundation cattle were acquired prior to the continental/dairy infusion(marble bone) in the US.

None of the defects the American Shorthorn Association recognizes have been found in the Native Shorthorn genetics, with the exception of clipper king who just so happened to phenotypically appear to be a roan Galloway and just so happened to have acquired TH, a defect only known to be in the Galloway breed prior.

I’m not sure it takes a geneticist to perform a little deductive reasoning.

 

[knabe]

It doesn’t matter what came from where.

Nothing is pure.

Pedigree tree is useful whether the same land race or not.

 

[librarian]

None of the defects the American Angus Association recognizes have been found in the Lowline Angus population- as all their foundation cattle were acquired prior to the continental/dairy infusion(marble bone) in the US.

None of the defects the American Shorthorn Association recognizes have been found in the Native Shorthorn genetics, with the exception of clipper king who just so happened to phenotypically appear to be a roan Galloway and just so happened to have acquired TH, a defect only known to be in the Galloway breed prior.

I’m not sure it takes a geneticist to perform a little deductive reasoning.

Of course I agree whole heartedly with this.
However, I still maintain that mutations are balancing responses to physical and environmental stress. Myostatin mutations rebalance the signaling pathways for regulating differentiation of muscle cells, fat cells and bone cells. There is a lot of Myostatin research going on in obesity, and diabetes treatment as well as fat burning, weight loss and and muscle building. This is not really an on off switch, but regulation of energy resources with trade offs concerning which cells differentiate and propagate.
I remember reading about Waygu and how weaning calves straight on to high energy diets caused cells that would ordinarily develop into muscle cells into fat cells. The calves are forced into insulin resistance and become essentially obese diabetics. But they are finished before they die of liver dysfunction or whatever diabetic condition they develop. With double muscling, the script is flipped. More muscle progenitor cells differentiate and the trade off is smaller adipocyte cells more densely packed into the space not taken up by extra muscle. As I am able to understand it...I don't understand it very well. Perhaps others can help unpack this paper in terms of what the adaptive trade offs are.
https://academic.oup.com/endo/article/157/1/282/2251849

 

[librarian]

And back to Heritage genetics regarding the phenotype remarks in the Denver bull thread. One cross of Haumont goes a lonnnng way.

 

[librarian]

The Conan Hypotesis actually seems to have some merit.
"In conclusion, our results suggest that myostatin endows skeletal muscle with high oxidative capacity and low fatigability, thus reg-ulating the delicate balance between muscle mass, muscle force, energy metabolism and endurance capacity."
https://www.researchgate.net/profile/Raphael_Denis/publication/263432884_Myostatin_is_a_key_mediator_between_energy_metabolism_and_endurance_capacity_of_skeletal_muscle/links/00b4953b126c59aa96000000/Myostatin-is-a-key-mediator-between-energy-metabolism-and-endurance-capacity-of-skeletal-muscle.pdf?origin=publication_detail

 

[Boreal]

The Th defect in Galloway and the one in Shorthorn are different - so the Clipper King theory is wrong.

There have been other defects found in heritage Shorthorns. That doesn’t mean they aren’t heritage. The origin of most defects pre date the herd books of the breeds that contain them, so little can be deduced re: purity and defects.

nt821 is an old mutation shared by Galloway and Angus, among others. It’ll be in lowlines.

 

[librarian]

The Th defect in Galloway and the one in Shorthorn are different - so the Clipper King theory is wrong.

There have been other defects found in heritage Shorthorns. That doesn’t mean they aren’t heritage. The origin of most defects pre date the herd books of the breeds that contain them, so little can be deduced re: purity and defects.

nt821 is an old mutation shared by Galloway and Angus, among others. It’ll be in lowlines.

I did not know this. It's very interesting. My total agreement was that there was a Galloway infusion in Clipper King of Bapton.

 

[librarian]

Got some pictures today of my Heritage Shorthorn acquisitions.

 

[librarian]

This was the only one in the pen of this phenotype. He is to be used on Galloway cows to breed Blue Greys. The theory being that mating different phenotypes produces more heterosis.

 

[librarian]

Paternal half sibs

 

[librarian]

These calves have been here a week. I'm sure the feed was much better at DMH. This is late cut prairie hay and the roan bull has definitely gained weight since coming here. They get all they want of this hay and mineral. The white bull has lost weight, or at least lost gut. Very fascinating how the genetic cards get dealt.