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Myostatin Mutations
Double Muscling

Myostatin - Double Muscling (DM or MYO). Myostatin mutations appeared relatively recent in history and were propagated by beef breeders selecting for increased muscle. The double muscling syndrome was first described in Durham Shorthorn cattle by the Englishman, George Culley in 1804 (hence today's EU / UK word for DM; "culard" or "cullard"). Normal cattle have active myostatin. MYO mutations reduce or stop normal myostatin protein production, affecting or causing unregulated muscle growth. Different myostatin variants produce different phenotypes, combinations & degree of symptoms. There are both advantages and disadvantages (and great variations in both) to consider when raising DM cattle. The issues to consider include the following:

There are currently 9 DM variants identified in cattle. They are still not well researched or completely understood. Most DM mutations originated in different breeds. Some are dominant and some are recessive; but most display incomplete penetrance, some interact with other genes, and with each other when combined. Selection pressure has dramatically affected their phenotypic expression, which varies between mutations, and can vary remarkably in the same mutation between breeds. Six myostatin variants are “disruptive” mutations, which cause the "double-muscling" effect results from enlarged muscle cells. Three are “missense” mutations, which increase muscularity due to the animal having more muscle cells.

Here is a table of the known DM variants and the breeds they are most often associated with:

hypertrophy mutation possible origin: but also found in:
C313Y disruptive Piedmontese
E226X disruptive Shorthorn Maine Anjou, Chianina, Speckle Park, Parthenaise
E291X disruptive Marchigiana
nt821
disruptive Belgian Blue South Devon, Blondes, Limousin, Normande, Shorthorn, Speckle Park, Angus
nt419 disruptive Maine Anjou Shorthorn
Q204X disruptive Charolais Limousin, Belgian Blue, Parthenaise
hyperplasia possible origin: has been found in a few:
D182N missense Maine Anjou
S105C missense Parthenaise
F94L conservative Limousin Aubrac, Shorthorn, Marchigiana

 

sharable infographic:
infographic


Research compiled from:
Haplotype diversity of the myostatin gene
among beef cattle breeds

Genet. Sel. Evol. 35 (2003) 103–118,
©INRA, EDP Sciences, 2003
DOI: 10.1051 /gse:2002038

  • A total of 678 animals from 28 breeds were used in this study; done in labs in Spain, France, Belgium, UK.
  • detecting the nine mutations affecting the coding sequence of the myostatin gene
  • Some mutations (disruptive nt821 and conservative F94L) are widespread across bovine breeds.

5 that disrupt the protein (nt821, Q204X, E226X, C313Y, nt419)
1 conservative mutation (F94L)
2 missense (S105C and D182N; results not shown)

4 Spanish breeds:
Asturiana de la Montaña (AM)
Asturiana de los Valles (AV), nt821, F94L
Pirenaica (PI) and nt821, F94L, nt419
Rubia Gallega (RG) nt821, F94L

12 French breeds:
Aubrac (AU)
Bazadaise (BZ)
Blonde d’ Aquitaine (BA)
Bretonne Pie Noire (BR)
Charolaise (CH) Q204X, F94L
Gasconne (GA) C313Y, F94L
Inra95 sire line (IN95)
Limousine (LI)
Maine-Anjou (MA) E226X, nt419
Normande (NO)
Parthenaise (PA) nt821, F94L, E226X, Q204X, nt419
Salers (SA)

2 Belgian breeds:
Blanc Bleu Belge Mixte (BBB mixte)
Blanc Bleu Belge culard (BBB)

9 British breeds:
Aberdeen Angus (AA)
Ayrshire (AY)
British Shorthorn (BS)
Devon (DE)
Galloway (GL)
Hereford (HE)
Traditional Hereford (HT)
Longhorn (LH)
South Devon (SD)

1 Italian breed:
Marchigiana

published online: May 2019

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