MYOSTATIN E226X – Busting the Myths

Myostatin E226X is a variant gene known to be present in the Shorthorn population in Australia and it seems to be generating a lot of myths around its effects. Whilst breeders will make their own decisions regarding the desirable gene frequency of E226X within their herd, it is important that they make these decisions based on objective information.

In this article we will attempt to bust the myths and shed some light on the Myostatin E226X variant gene and its effect on Shorthorn cattle.

The cause of most of the myths seems to stem from one essential problem.

When breeders think of the Myostatin variant gene it tends to conjure images of the Belgian Blue type animal. Whilst this may be understandable, it just isn’t correct.

Myostatin variant genes occur in many breeds from Angus to South Devon to Limousin to Belgian Blue. Much of the visual muscle that is observed in these breeds is the product of genetic gain, not just a Myostatin variant gene.

So lets start busting some of the myths.

MYTH 1: That breeders can visually appraise the Myostatin status of Shorthorns.

Some breeders are reporting they know that certain sires are Myostatin carriers based on how the animal or progeny look.

Unfortunately, most of these bulls have not yet been tested for a Myostatin variant. Certainly, some of the mainstream sires that breeders have categorically stated are Myostatin E226X carriers, have since been tested free.

The FACT is, it is not possible to determine visually whether a Shorthorn animal is a Myostatin variant carrier or not. Only DNA testing can determine the Myostatin status of an animal.

MYTH 2: All Genetic Defects are Bad.

If we assume this logic to be true then we would have to conclude that the Poll gene is bad, given it is also a genetic defect. So is blonde hair in people and yet as we all know, blondes have more fun.

In FACT, if you believe in Charles Darwin’s theories or practice any population genetic principles, then you must first agree that gene mutation is often a critical function for a species to adapt to survive in a changing environment. Not all genetic defects are bad, many are extremely beneficial.

MYTH 3: Myostatin E226X is the cause of many production issues.

Breeders are associating the Myostatin E226X variant gene with all sorts of production problems such as dystocia, increased birth weights, bad feet, lower temperament, decreased fat, extreme muscling and decreased marbling.

If only one gene could be influenced to correct all these traits! How easy would cattle breeding be then.

In FACT, there is currently no real evidence to support any of these claims.

There are 9 common Myostatin variant genes in beef cattle, of which 6 are considered disruptors. Every Shorthorn Beef animal DNA tested by Neogen Australia is tested against all 6 of these disruptor variants. Only the Myostatin E226X variant has been observed in Shorthorns in Australia.

The effects of the variant gene E226X on any phenotypes have not been recorded in sufficient numbers to determine statistically, with any accuracy, if E226X will have any real effect on any specific phenotypes.

Importantly though, the key traits that breeders are concerned about are all measured through Shorthorn Beef Breedplan, therefore any extreme phenotypes would be evident in the reported EBV’s. If breeders are looking to improve calving ease, bend the growth curve, improve fat depth or marbling they can achieve genetic gain through appropriate selection of EBV’s, regardless of the Myostatin status of the animal.

MYTH 4: Visual muscling in Shorthorns is directly related to Myostatin E226X.

Some breeders are avoiding using Shorthorns with above average visual muscling because they believe that those animals are Myostatin E226X carriers.

Our concern is that breeders are excluding genetics they would otherwise consider desirable. There are known Shorthorn genetics that exhibit excellent visual muscling and are free of the Myostatin E226X variant gene.

In FACT, of the Shorthorn animals currently tested for Myostatin, 67% of the animals have tested free of the variant gene. That is not representative of the overall Shorthorn population as it is understood that the animals are only tested because breeders believed that they displayed a phenotype which they considered to be representative of Myostatin carriers. So, most animals that breeders consider likely to be Myostatin carriers are actually free of the variant gene. You just can’t pick a carrier animal visually.

MYTH 5: Myostatin variant genes reduce eating quality.

Some breeders are concerned that Myostatin variants will reduce marbling and therefore reduce eating quality. Again, there simply isn’t yet enough information to know how the E226X variant will interact with marbling, if at all.

In FACT, whilst it is reported that other Myostatin variant genes have some diminishing effect on marbling in other breeds, it also reported that for every degree marbling diminishes, tenderness increases, with the net effect that eating quality is not diminished at all. Again, marbling is measured within genetic evaluation for Shorthorns, so breeders looking to make genetic gain for marbling within their herds can select for increased marbling through appropriate selection of IMF% EBV’s.


Here is what we know about the Myostatin E226X variant.

  1. Not all genetic defects are bad.
  2. You just can’t pick an E226X carrier animal visually. Anyone who says they can is either a clairvoyant or extremely optimistic about their ability. Only DNA testing can tell you which animals are carriers and which animals aren’t.
  3. Many of the Shorthorn sire lines commonly believed to be carriers are testing free. Again, you just can’t pick a carrier visually.
  4. Visual muscling in Shorthorns is a quantitative genetic outcome, not a qualitative one. In other words, it is affected by multiple genes, not one gene like E226X.
  5. The same is true for traits such as Calving Ease, Birth weight, Condition score, Marbling, Hoof structure and Temperament. Breeders looking for solutions to these production issues are going to need to achieve genetic gain through traditional selection methods. There is no silver bullet, like excluding the E226X variant, that will correct these issues.
  6. The only way breeders are going to be able to make informed decisions regarding the Myostatin E226X gene frequency within their herds is through DNA testing to know which animals are carriers and which animals are not. Any other method will be unsuccessful.
  7. Breeders are avoiding visually muscled Shorthorn genetics because they suspect that they are E226X carrier animals. In most cases all they are doing is reducing their capacity for genetic gain in this trait. Again, you just can’t pick a carrier animal visually. Only DNA testing can confirm an animals status.
  8. There are 9 common Myostatin variant genes. None of these work exactly the same as another. We just do not have enough tested Shorthorn animals to know exactly what phenotypic responses we can expect from E226X carrier animals. It is likely that for many markets, one copy of the gene may be considered favourable, for other markets unfavourable. However, for all markets, the traits will be best managed through appropriate EBV selection.

Hopefully, this will help to bust some of the myths that currently surround the E226X variant gene for Shorthorn breeders. In the near future, Shorthorn Beef will be able to display the testing results on the website for breeders. We respect each breeders right to choose to regulate the frequency of the Myostatin variant gene E226X within their own herds, however it is important that decisions are made objectively. As we know more regarding the E226X variant, we will certainly keep breeders updated.

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About Shorthorn

The Shorthorn breed is truly unique, from their distinctive roan colour, to their rich breed history and most importantly, the wonderful community of breeders, there is nothing else quite like a Shorthorn.

The key to the Shorthorn breeds advantage lies in their balanced genetic profile, driven by market participation that has been developed and refined, after more than 200 years of genetic selection under Australian conditions.

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