Ahhh...
Words mean things and we have a definitional issue.
There are a very wide variety of mutations in the genetic code that impact muscularity in mammals. Some of these begin expressing themselves in utero. Some outside the uterus.
Traditionally, "double muscling" and "muscular hypertrophy" are really (!) bad words in terms of breeding functional cattle. To be 100% clear, any animal carrying disruptive variants of the myostatin mutation (see below for additional information) has no (!!) role in our breeding program, nor should it in anyone breeding maternally-oriented cattle.
Any mutation that expresses after the calf is born does NOT affect calving ease and is considered a 'missence variant'. The mutations that begin expressing themselves in utero that are the problems; they are 'disruptive variants'. F94L (commonly in Aubrac and Limousin cattle) is a 'missence variant' in the world of myostatin mutations.
Quoting directly from the Igenity "results key" (click
here for the info; see the 2nd page)
"Myostatin, as a part of the Igenity Profile, analyzes for nine different variants of the myostatin gene, even though some may not be found in all breeds. Six variants are classified as "disruptive;" these cause muscle hypertrophy (double-muscling), larger birth weights, increased dystocia and enhanced tenderness. Three myostatin variants are referred to as "missence," and will increase muscularity and reduce external and intramuscular fat, with no change in birth weight. For all myostatin variants one copy is intermediate."
Disruptive Variants:
C313Y (commonly associated with Piedmontese)
E226X (research ties this to Maine-Anjou)
E291X (commonly found in Marchigiana)
nt419 (research indicates this is commonly affiliated with Maine-Anjou cattle)
nt821 (research commonly ties this to Belgian Blue, Blonde d'Aquitaine,
Limousin (click here for more info) and South Devon cattle; of note, this type exists in some registered Angus cattle -- see
this fact sheet for additional information)
Q204X (research ties this to
Charolais (click for more info) and Limousin)
Missence Variants:
F94L (commonly in Limousin and Aubrac)
D182N
S105C
F94L (and a few others) do not begin expressing themselves until the calf is on the ground. As a result, the calf will be of a normal size with typical amounts of muscling. In these instances, the enhanced muscling doesn't begin to express until the calf is on the ground, typically (at least in Aubracs) around 3-4 weeks of age.
There are many (!) types of muscular hypertrophy being uncovered by researchers around the world on a regular basis. The ones above are the ones available for DNA testing via Igenity (Neogen / Geneseek). Other labs may offer testing for other types of myostatin mutations. Google is your friend for more info...
Here is a decent primer on some of these issues on the South Devon website, including a detailed bibliography for additional reading -->
click here
NOTE --- THE IGENITY QUOTE ABOVE DOESN'T REFERENCE THAT SOME OF THE MUTATIONS RESULT IN MORE MUSCLE FIBERS THAT ARE THIN, OTHERS RESULT IN THE SAME NUMBER OF MUSCLE FIBERS, BUT THE FIBERS ARE THICKER. THICK MUSCLE FIBERS ARE HARDER TO CUT AND THEREFORE RESULT IN TOUGHER BEEF. IF YOU WANT TENDER BEEF, FIND A MUTATION (like F94L) THAT RESULTS IN MORE THIN MUSCLE FIBERS. THE IGENITY DEFINITION (imo, wrongly) ASCRIBES TENDERNESS TO ALL DISRUPTIVE VARIANTS AND NONE TO THE MISSENCE VARIANTS. IT HAS BEEN OUR EXPERIENCE THIS ISN'T ACCURATE -- SOME DISRUPTIVE VARIANTS ARE TOUGHER AND SOME MISSENCE VARIANTS ARE MORE TENDER. F94L CARRIES THE WONDERFUL DISTINCTION OF BEING BOTH A MISSENCE VARIANT and RESULTING IN MORE LONG, THIN MUSCLE FIBERS.
While not definitive, this is the most wide-ranging research I've seen in terms of the numbers of breeds covered.
