The double muscling syndrome myostatin is not a new phenomenon and was first documented 200 years ago in Durham cattle by Englishman George Culley (hence the synonym culard). In cattle, double muscling is largely due to the loss of function of the myostatin gene (GDF8), which, in turn, is due to a mutation in the gene. The identification of the gene has been an important find, as it represents one of the first genes identified with large effects on important traits such as meat yield and quality.
The double muscling syndrome myostatin is not a new phenomenon and was first documented 200 years ago in Durham cattle by Englishman George Culley (hence the synonym culard).
In cattle, double muscling is largely due to the loss of function of the myostatin gene (GDF8), which, in turn, is due to a mutation in the gene. The identification of the gene has been an important find, as it represents one of the first genes identified with large effects on important traits such as meat yield and quality.
Several cattle breeds harbour mutations in the myostatin gene and show a hereditary muscular hyperplasia (double-muscled cattle). Indeed, in Ireland, case variants have been successfully identified in Angus, Belgian Blue, Charolais, Limousin and Simmental populations, or five of the six main beef breeds (all except Hereford).
With advances in genomics and genotyping technology, DNA testing for myostatin is now easily available. For pedigree breeders, knowing the myostatin status of animals within their herds, along with the myostatin status of sires they choose, is becoming ever more important criteria to take into account when deciding on choices and options to make in their breeding programmes.
What are myostatin genes?
The myostatin gene (GDF8) is found in all mammals and influences the production of a protein that controls muscle development.
Several mutations of the gene produce proteins that are less effective at controlling muscle development, which results in increased muscle mass in cattle. There are nine known mutations of the myostatin gene in cattle, some of which are breed-specific and others which affect more than one breed.
Six of these variants are classified as disruptive – nt821 del 11, Q204X, nt419, E226X, C313Y, E291X – and three other variants – S105C, F94L, D182N – are referred to as missense.
The six disruptive myostatin genes cause muscle hypertrophy (double-muscling) in cattle, but are also associated with larger birth weights, increased dystocia and enhanced tenderness.
The three missense myostatin genes will increase muscularity, but not cause double-muscling, and reduce external and intramuscular fat, with no change in birth weight.
Myostatin genes are recessive and thus only come to their full expression and affect when an animal carries any two copies. So, for the full expression of double-muscling to occur in cattle, there has to be a complete absence of functional myostatin protein, which requires that both copies of the myostatin gene be defective (disruptive).
An animal inherits two different genes; one from its mother and one from its father. Recessive means that if one myostatin gene and one normal gene are present in the same animal, the myostatin gene will be suppressed by the opposing dominant non-disruptive gene inherited from the other parent.
For example, when one myostatin and one normal gene are passed on to a calf, the calf may show some extra muscling, but will never show extreme muscling from having only one myostatin gene. The normal gene will overpower the myostatin gene and stop extreme muscle growth.
Outcomes when breeding with ‘none’, ‘carrier’ or ‘double muscle’ animals With DNA testing, cattle can be classified based on their myostatin results as:
0 – None (N): None of the possible myostatin variants. 1 – Carrier (C): One copy of the myostatin variants. 2 – Double muscle (DM): Two copies of the myostatin variants.The following are the different outcomes when breeding with none (N), carrier (C) and double muscle (DM):
1 What happens if you breed an N animal to another N animal?
100% of the calves will be carrying N. They are all free of the myostatin gene. - No double muscled calves can come from this pairing.
2 What do you get if you breed an N (0 copies) with a C (1 copy)?
There is a 50% chance of getting N (no copies). There is a 50% chance of getting C (1 copy, a carrier). There is a 0% chance of getting DM (a double muscled calf). - No double muscled calves can come from this pairing.
3 What do you get if you breed a C to a C?
There is a 25% chance of getting a DM (two copies of the myostatin gene) – this calf will be double muscled. There is a 25% chance of getting N (no copies).There is a 50% chance of getting a C (carrier of 1 copy). - This combination will result in 25% of calves being double muscled.
4 What do you get if you breed a C to a DM?
There is a 50% chance for DM (2 copies of the myostatin gene) and thus double muscled. A 50% chance for C (carrier, 1 copy). - This combination will result in half of all calves being double muscled.
Benefits and risk with myostatin
If we examine the benefits, myostatin genes have been proven to improve all the economically relevant carcase traits. Additive effects are seen for increased carcase and meat yield and a higher proportion of high valuable meat cuts in the carcase, improved muscle to bone ratio and dressing percentage.
Meat from double muscled cattle tends to be of better quality due to a combination of increased tenderness, reduced fat content and a higher proportion of polyunsaturated fats.
Additionally, cattle with the myostatin variants have greater feed and lifetime production efficiency, thereby conferring economic and environmental benefits.
In quantifying the improvements in retail beef yield and meat quality, research studies have shown significant advantages to be gained even in cattle with only one copy of the myostatin gene (heterozygous) present.
At the same age, these cattle have 1% to 3% higher dressing percentage, 3% to 10% more lean meat yield and 13% less fat relative to conventional contemporaries.
Meat is more tender in relation to both overall tenderness (shear force) and tenderness due to reduction in meat toughness from connective tissue and collagen content.
From a disadvantages viewpoint, care should always be taken when selecting for and breeding with double muscled animals due to calving, fertility and fitness concerns. These difficulties can be manifested within a herd, if animals carrying nt821 and Q204X are mated to animals that are carrying or are homozygous for the double-muscled mutations.
Given that some of these combinations will result in half of all calves being double muscled, this heightens the potential of calving problems due to increased birth weight and subsequent breeding problems in the herd females, such as lower milk and fertility.
Collectively, the research work on this topic in France and Australia shows that the incidence of dystocia increases with calves homozygous for the double-muscled mutations, but heterozygous calves did not experience any calving problems.
Also, cows heterozygous for a myostatin mutation (one copy) had similar conception rates, calving percentages and milk production when compared with normal cows.
Thus, for some beef breeds, undoubtedly there are advantages to be gained from breeding heterozygote animals due to their increased retail beef yield and production efficiency.
Once a pedigree animal is DNA genotyped, for instance as part of the BDGP scheme, its myostatin gene status can be retrieved.
Knowledge on the myostatin genotype is an additional bit of information that may help decision-making, especially with regard to specific matings within the herd and also to potentially avoid procreating animals with calving and fitness related problems.
The use of the myostatin genes in pedigree beef herds, if managed successfully, could have profit potential, but will need careful monitoring with rigorous myostatin gene testing.
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