Oops! It appears that you have disabled your Javascript. In order for you to see this page as it is meant to appear, we ask that you please re-enable your Javascript!

Is myostatin the catalyst behind the “standard” birds?

Is myostatin the catalyst behind the “standard” birds?

Published: BVA magazine 01-10-2008
on-line: 11-11-2008

By Dirk Van den Abeele

Who does not know them, the “long feathered” or standard A. roseicollis? They are usually the champions of the show and excel in size and colour. For this reason this type of bird is highly desirable to most breeders. The difference with the “normal” A. roseicollis is significant, the “long feathered” birds literally tower above the “normal” types. When in 1992 these birds were first displayed on the BVA show this generated, as per usual in the bird world, the usual distrust and gossip, wild assumptions and doubt. For the bird enthusiasts are notoriously conservative and new things, especially when they cannot be explained easily, usually encounter a lot of prejudice. Those who could acquire such a “long feathered” bird and bred it were very happy. Others who did not own these birds were cautious.

The origin of these birds lies in the Netherlands. Jac De Jong can justly be called one of the first breeders of these birds. A multitude of theories exist regarding the cause of this “long feathered” type. Combinations with the subspecies Agapornis roseicollis catumbella, special nutrition, hormones, even the polyomavirus were named as the possible cause of this type of bird. Jac de Jong was and still is very open about this : selection of the best young to build a complete quality population step by step. Because these birds’ prices were within everyone’s budget, this type has replaced the smaller “normal” wild type in most collections over the course of a few years. The old protests have died down and most of our breeders consider themselves lucky with their “long feathered” roseicollis. After only seeing this bird type in the green base type during the starting phase, it has later on spread to most mutations. Breeders now agree that once you have access to this “blood line”, this bird is easy to breed.

The fact that certain birds suddenly become bigger is not new and is definitely not limited to Agapornis roseicollis. Everyone probably also knows budgerigars [Melopsittacus undulatus]. For this species there are also two distinct types: the normal type, as found in their natural habitat in Australia and the large types sometimes referred to as “English” budgerigars because the first larger types were bred in England around 1910. The zebra finches [Taeniopygia guttata] also have similar specimens. The birds are described over the years in different ways: intensive, long feathered, of the new type, etc.

The most common is the description “the long feathered roseicollis”. But because this type does not always have a somewhat longer feather and the name gives the wrong impression for non-experts, we adopted the name “standard type (ST)” for these birds a few years ago, similar to the larger types of budgerigars.
Still the question remains how it is possible that certain birds now become so much larger. Everyone knows that domesticated bird species, thanks to better nutrition and selection, have become bigger. But why does this advance faster for one species than for the other? We have for generations been breeding A. nigrigenis, A. personatus, etc, why has the size for these birds not changed as much as for A. roseicollis? How is it that, when one does not start with a breeding pair where one bird is a standard bird, that even after years of selecting the result is not the same as when one starts with a breeding pair where one bird is a standard bird and the other a normal wild type?
All of this combined clearly indicates that there must also be a genetic cause, or as the amateurs would put it: “you must have access to the bloodline”, in other words there is/are definitely mutation(s) involved!

There is still much doubt about the correct manner of inheritance and about which genes are involved in this mutation. It is a fact that if we start with a “standard bird” and pair it with a bird of the smaller wild type, we could if we are lucky already breed larger types after about two generations. One of the first articles on this subject was an article by Herman Henderickx in the BVA magazine in June of 1996. In this article Herman described his own breeding experiences with these birds and I quote literally :
“With regard to the inheritance: this is quite another issue ! According to some it inherits recessively, whereas according to others the inheritance is intermediate, i.e. with an intermediate type. Assume that we start with a long feathered male or hen (it does not matter which) and we pair these with a common bird then we would expect the young to all be half long. In reality this is not the case. A small percentage of these young are still normal, they are not exceptional with regard to size. For the intermediate type that is sometimes called “split” we already see that the head is more pronounced and flatter, also that the colour of the mask is warmer. If we now pair two such birds then for some couples we can expect everything: normal, half long feathered, long feathered, large birds with a small head, small birds with a large head, and finally very small birds with whom we should definitely not breed. Other couples in turn can produce better offspring, in which the percentage of “small ones” is significantly less. From the pairing: long feathered x half long we can in my opinion get the best young, from which we will breed the largest number of long feathered birds that will approach the intended quality the most.”

Own experiences with this type of roseicollis are comparable to the information in Herman’s article. I quote from an article written by me in 2000 :
“My first long feathered birds were obtained from two birds I had bought in retail, the bird’s mask was a bit redder than normal but size wise it was normal. When I enquired I found out that they came from Jac De Jong, who took them to the retailer because they were “not good enough”. In the first nest I had a long feathered bird (one out of four young) but unfortunately it died after a few months. In the second nest I luckily had another long feathered young (also one out of four young) and this one stayed alive. Then I bought a half long feathered bird from Herman Henderickx and paired it with my bird. Up till now I have bred about 10 long feathered birds from this pair (a ratio of 1 out of 3). I have also combined a long feathered bird with a “normal” roseicollis and after three generations I have already bred long feathered young out of these birds, although they are still smaller than the young from the first set. I can guarantee you that even now I still need to make the proper selections.”

If we would now, 8 years later, compare the birds which were then considered to be “long feathered” to the large specimens we see today, then we would see that the birds have evolved size wise. As is the case in budgerigars, the difference between the “standard type” and the nominal type has become bigger over the years.
Because of these experiences we suspect that we are dealing with an autosomal recessive inheritance. Because for these birds not only the size became bigger, but the paws have also become thicker, the colour a bit more intense, we decided that more than likely multiple genes are involved in this mutation and the term “multi factoral inheritance” can definitely be used. But now there are justified reasons to assume that these thicker paws and the larger size can still depend on a single gene.

Myostatin
Myostatin is a protein involved in the production of muscle tissue. The task of myostatin is to limit the muscle growth at a certain point: the higher the concentration of myostatin in the body the less the growth of muscles.
Myostatin and the encoding gene were discovered in 1997 by Alexandra McPherron and Se-Jin Lee. These scientists managed to deactivate the myostatin gene in mice. As a consequence these mice developed about twice the amount of muscle mass than is normal. Later on it was discovered that the same gene is also responsible for the “double muscled” cattle and sheep which we have been breeding for years. In sheep this mutation is called “callipyge”. Because the myostatin gene can easily be traced it was soon discovered in various mammals, fish and … in birds.

It is suspected that over the course of the evolution this gene has spread in most species, even in humans. In 2004 a boy was born in Germany who was significantly stronger than his contemporaries. Research has shown that in this boy both myostatin genes – on each chromosome – had mutated. His mother, who used to be an athlete, was found to also have a faulty gene. In 2007 the gene was discovered in dogs, more specifically in whippets, where myostatin appears to be responsible for specimens who are significantly more muscled and larger than other dogs.

As a result it is now suspected that myostatin might also be responsible for the “standard” budgerigars and the “standard” roseicollis!
Further research into the myostatin gene in double muscled cattle has taught us that when combining such a double muscled cow with a normal cow the F1 offspring always display a muscle mass which is located somewhere between the two parent animals.

The situation is comparable to what we see in the standard A. roseicollis: combinations of F1 offspring have about 25% normal animals, 50% intermediate types (similar to the F1 offspring) and about 25% animals that are “double muscled”. With each generation of “double muscled animals” an increase of 10 to sometimes 30% of the muscle mass is observed, as is the case with our “standard” roseicollis.

It becomes even more interesting when we investigate the genome of these animals. As a result we see that the gene in double muscled cattle has a penetration level of about 95%. This means, put simply, that for the offspring where the myostatin gene has mutated on both chromosomes (animals that are homozygote for myostatin) about 5% are intermediary muscled. This variable expression shows that the gene is influenced by pleiotropy and this in turn means that the other mutated factors present also affect the expression of the myostatin gene.

If we apply all of this to our standard roseicollis we notice that for the combination of a standard green A. roseicollis with a normal (small) wild type the breeding results are comparable to the breeding results in double muscled cattle. If we combine a standard roseicollis with other mutations the breeding results also display a variable expression, as is the case in cattle. Breeding in the standard type is much easier in SL (sex linked) mutations that in some autosomal recessive mutations, so also for our birds the additional mutations influence the expression of the standard type.

In the standard budgerigar we have a similar situation. Mr Jan Bouwmeester, a respected judge and passionate budgerigar breeder, bought his first recessive pied budgerigar in 1978. He wanted to pair this recessive pied mutation with a standard bird and see how long it would take for this pair to breed young with the size of standard birds. The recessive pied bird was linked in 1979 to a standard bird and the first young, all green/recessive pied, displayed a minimal improvement in size. Mr Sieb Harkema from the province of Groningen had a similar combination at that time as well and Mr Bouwmeester received a young from him from this “special” breeding pair, a mauve yellow mask / recessive pied hen. This young did not display an improvement in size. Mr Bouwmeester constructed a breeding pair consisting of the young hen from Mr Harkema and a young male from his own “special” parent pair. He started a line and – luckily for us – kept a detailed diary. As a result we can now gratefully use his information. After about 9 generations the first recessive pied birds were born that are equal to the average sized birds. The following year recessive pied birds were born that can be considered top birds where size is concerned. It is important to know that these recessive pied birds are always born out of splits.

Mr Bouwmeester even compared the skull size of the birds. Dead birds were dissected and the skull was completely analyzed. The measurements showed that the difference in skull size (bare bone structure) between a normal wild type and a size bird is barely 10% during the whole process. As a result Mr Bouwmeester concluded that the larger head in the standard budgerigar is probably caused by the feathers and the way these feathered are implanted. Why the feathers are implanted differently does become apparent: when the muscle mass of the skull becomes larger, it will be more round and as a result the feathers will of course be implanted differently. All these results clearly indicate that myostatin is involved.

Another example of increased muscle mass can be found in the paw thickness in roseicollis. The normal wild type can easily be ringed using a size 4.5 mm but for standard roseicollis a size 5mm needs to be used.

Of course the question whether the length of the feather is connected to myostatin remains unanswered. Not all standard birds have longer feathers. A lot of standard birds have well connecting normal feathers. Furthermore we see in various other bird species that mutations occur in the feather which are in no way connected to larger type birds. As a result I suspect that the various feather types are caused by a separate mutation.

The question whether myostatin is involved in the sometimes diminished breeding results in standard birds I would also answer with no. I think that the large percentage of inbreeding is the culprit. Many breeders keep using the same bloodline for years and / or buy their birds from the same breeders. Most of the time they also have birds from related bloodlines and this results in inbreeding. The danger of inbreeding is that a lot of hidden defects become visible: heterozygotes become homozygote for a certain characteristic, with all its consequences.

Bibliografie

  1. McPherron AC, Lawler AM, Lee SJ. Regulation of skeletal muscle mass in mice by a new TGF-beta superfamily member. Nature 1997;387:83-90. PMID 9139826.
  2. Z. Gu*,†,¶,1, Y. Zhang*,†,1, P. Shi‡, Y.-P. Zhang‡,§, D. Zhu*,† and H. Li**, Comparison of avian myostatine genes. International society for animal genetics, Animal Genetics, 35, 470
  3. V.K. SAXENA*, P. SINGH, A.B. PRAMOD, K.A. AHMED, M. SAXENA and R.V. SINGH, analysis of Myostatin gene revealed, species specific sites in turkey and chicken, 2005, XVII th European Symposium on the Quality of Poultry Meat Doorwerth, The Netherlands, 23-26 May 2005
  4. Rodgers BD, Roalson EH, Weber GM, Roberts SB, Goetz FW. “A proposed nomenclature consensus for the myostatin gene family.” Am J Physiol Endocrinol Metab 2007;292(2):E371-2. PMID 17003236.
  5. McPherron A, Lee S (1997). “Double muscling in cattle due to mutations in the myostatin gene”. Proc Natl Acad Sci U S A 94 (23): 12457-61. PMID 9356471. 

 

2 Responses to Is myostatin the catalyst behind the “standard” birds?

  1. linda says:

    You are the best!!

  2. Sherjil says:

    Hi Dirk;
    This is one of the best explanation I have read for the occurence of large sized birds in captivity.
    Question :

    1) Is myostatin responsible for extra muscle mass in broiler chicken as well ?

    2) Are there similar genes indetified which are responsible for increased skeleton size e.g.great dane dogs , aseel chicken etc

    3) What is required to make such “standard” size birds a better flyer like “normal” size birds ?

Leave a Reply

Your email address will not be published. Required fields are marked *

This site uses Akismet to reduce spam. Learn how your comment data is processed.