The distinctiveness of the “Intensive” mutation

The Intensive mutation display some absolutely unique aspects, never encountered in any other species. Before going into the mutation description we should tell something about the original wild-type bird.

Canary (Serinus canaria), originating from the Canary Islands, the Azores and Madeira, bears a green plumage because of the presence of black and brown melanins and of lipochromes, namely yellow carotenoids.

We will focus our attention on the aspect so called category, that is the distribution of carotenoids and the plumage structure.

The carotenoids, in the wild-type canary bird, do not reach the outer edge of the feathers, originating a whitish fanlight, like a lunette, and the feathers have a regular structure, as expected in a wild-type animal. This whitish fanlight let us think to frost crystals; so the presence of the fanlight is called frost, and the wild-type birds are called frosted (or buff in the yellow series, or non intensive in the red series of canaries). This means that the wild-type canaries belong to the Frosted category. Different languages have different words for this category; for example the Flemish say schimmel (mould), word found also in other languages, in spanish they use nevado (snowy).

It is important to underline that the presence of this frosty white lunette can vary along the body. There are areas, called marking zones, which lack the whitish lunette, the feather is indeed entirely saturated with carotenoids and the colour appears more intensive. These are the facial mask, the epaulettes, and the rump.

Vice versa, there are body regions in which the frosty effect is stronger, becoming more evident, giving the feather a lighter colour. These areas are the neck and, mainly, the ventral zone. This situation is nor weird or rare, in that it is spread in many species in a more or less marked form.

The Intensive mutation is a shocking distinctiveness. The name derives from the evidence that the colour is more concentrated and exaggerate and so more intensive.

This mutation acts shortening the barbs and reducing the other epithelial structures, the beak and, more evidently, the feet flakes and nails.

The vane reduction shortens and narrows slightly the feathers (even if it is usually referred to as shorter feathers only). This reduction causes an increase in carotenoids concentration, giving a stronger colour. Many people think to an increase in carotenoids quantity, and indeed this hypothesis is possible but not probable.

A scheletric reduction has been hypothesized, but it is not verified, even if the body structure appears thinner and gives the impression to be smaller. The foot also presents tarsus, metatarsus and fingers thinner, but this appearance depends on the reduction of the flakes. Indeed the morphology is more related to the plumage than to the bones.

We have to take into account that many genes control plumage, in fact we can observe intensive birds with very long and rich feather (after all the intensive mutation acts on the barbs, not on the rachid) even if the mutation has its maximum expression, namely without any residues of whitish fanlights, and we can have buff birds with narrow adherent feathers, even if not like the intensive ones. The difference between intensive and frosted birds is really appreciated in a general common aspect and better in between a brotherhood. Anyway this is a really drastic mutation with a strong effect.

The genetic behaviour is autosomic, dominant and sub-lethal, there is variable expression and, possibly, an additive effect due to the presence of interfering genes. For example, there is an interference with the sexual dimorphism and female subjects appear less intensive than males, because they very often present traces of the frost, not common in males.  Actually also the wild-type frosted canaries show a stronger frost in females and the marking zones are less evident. It is noteworthy that the marking zones are called intensive, but the structure of the feathers appears normal, not shortened, so in this case there is a saturation in carotenoids not related with the intensive mutation.

The variable expressivity is related to frost traces that can be present especially in the areas in which the frost is stronger in the wild-type: the neck and the ventral zone; while they are never present in the marking zones.

Homozygous subjects, called double intensive, appear stunted, very thin, the extreme reduction of the vane allows to see the skin near the eye. It was erroneously hypothesized that some feathers were missing, but it is only an impression. Even the feet appear thinner because of the reduction of flakes. Nails and beak are affected too.

We also talked about lethality of the homozygous, but this does not correspond to the truth.

Up to this point it would seem to be a very rare and violent mutation, but not altogether exceptional; the exceptionality, or rather extraordinary uniqueness, appears in the couplings. After the appearance of the intense mutation, it seems that the domestic frost has undergone a variation, probably a real mutation, somehow inverse to the intense and degenerative, it would then be no longer the wild-type buff, but rather a pseudo wild-type, only for its phenotype or appearance.

I hypothesize that the intensive mutation is paramutagenous, capable of inducing a mutation in the frosted and of opposite sign to the intense.

If the domestic buff is coupled in purity the frosting is accentuated, the carotenoids weaken and the plumage becomes excessive. Going on with repeated coupling the phenomenon is accentuated. One can have subjects so faded that they are almost whitish.

A further oddity is that with the mixed coupling: intense heterozygous x frosted the degenerative phenomenon does not happen; in fact there is a 50% of intense heterozygotes and a 50% of frost in excellent balance, without degenerative appearances. In practice, the Canary species in the domestic state is split in two and the buff needs the intensive to get balanced.

Certainly this need is not present in nature, where the intensives do not exist, and the frosted mate in purity without any problem. After all, the wild-type form is usually the best because of natural selection and does not need anything else.

I point out that there is some strain in the domestic breeds that does not present the degenerative aspect, like the Malinois singing breed, but I do not think it is a coincidence: it does not include intense subjects, since the Malinois are all frosted. After all, this is a strain that remained separated from the other canaries due to the need for a particular selection for singing.

In the past I had thought that the intensive mutation had induced the inverse mutation in the cytoplasm. However, today I think it is more likely that the nuclear gene affected by the mutation has been further mutated.

However, there are aspects that suggest a cytoplasmic involvement, as we will see.

How to explain the balance in mixed mating? I think the reason could be not strictly genetic, because of the constancy of the effect, but of biochemical type, perhaps linked to a phenomenon similar to heterosis, I underline similar not exactly identical.

On the heterosis, I do not agree with the theories that look for a genetic explanation, because if this were the case, the heterosis should be kept in part of the offspring. I think the explanation should be rather biochemical.

I have to say that I believe in the theory of Shull, based on the initial cytoplasmic stimulation, although I believe that certain heterozygous conditions can interfere, again for biochemical reasons, like the production of different enzymes.

In support of this thought I can say that the results of the mixed combination of intensive heterozygous x buff are, even if very little, better when the female is intensive. Perhaps we could think of a greater initial stimulation when the cytoplasm of the egg is of an intensive subject and the sperm of a buff.

I repeat that the coupling with buff male and intensive female is only of very little better quality and the inverse is fine too. These are trifles, like having less traces of frost in the intensive. Obviously the quality of the subjects used is paramount.

It should however be noted a further strange effect, but linkable to previous arguments, that is by coupling intensive x intensive both heterozygotes, we have 25% of intensive homozygotes already described, 25% of frost, but they usually appear of inferior quality to those born of mixed mating. They tend to excess almost like those born from a mating in purity. In addition there is 50% of intensive normal heterozygotes usually excellent. I point out that the quality of the intensive heterozygotes born from a coupling intensive X intensive both heterozygotes, is generally higher than average.

It is noteworthy that the intensives born from the coupling in purity almost never show traces of frost, especially in males, even when such traces were present in the parents. It is the only exception known to the golden rule of not pairing subjects with the same defect so as not to accentuate it in the offspring.

For further comments on the characteristics and selection of the categories, please note that there is also the mosaic and that it is important, I suggest to read other publications both in paper and informatic, also present in this website.

I would like to underline once again that all the finches correspond to the buff (to a normal buff of wild-type characteristics of course) even when they resemble the intense or the mosaic. There were several very serious misunderstandings, for example the male of the Red Siskin (Spinus cucullatus) was considered intense, while it is only similar concerning the saturation of the feathers by carotenoids, but the structure is normal, moreover there is a very strong concentration of frost in the ventral zone which becomes whitish. Furthermore, a sub-lethal mutation cannot be wild-type!

An opposite mistake led to consider the female of the aforementioned species a mosaic, considered the origin of the mosaic category, a thesis that I have cut short in various locations, even on this site.

In nature, diversification into categories does not exist, and in the domestic state there is only in Canary and I hope that it will stay there only, given the problems involved. In order to understand each other, a strain split into two categories that need each other, would not be usable for a re-introduction in Nature.

Giovanni Canali    

 

Side note by Dr. Pasquale De Luca

Genes usually encode proteins, which play a role in the functioning of cells and organisms, and in turn are the true culprits of the phenotype. The proteins that take part in biochemical reactions are called enzymes. We could assume that a mutation occurred in an X gene that controls the length of the beards. The corresponding enzyme does not work like the original one and causes shorter beards to form. This mutation could be due to the "Intensive" phenotype. Surely at the time the new individuals, with bright colors, were preferred and selected (not in Malinois that maybe later did not sing better).

Suppose that, during the initial phases of the selection, a new mutation (buff in the canary) was generated in the X gene, which does not directly affect the length of the beards, but which changes in some way the control of the enzyme activity, maintained instead in the "intensive" version. Before formulating our theory we must remember that in the cytoplasm of the egg the female accumulates a lot of reserve substances that serve at the beginning of the life of the embryos, including many already prepared enzymes and many messenger RNAs to form new enzymes (in the first hours after fertilization the only true activity of embryo DNA is duplication to form many new cells, embryonic genes start to work later).

Then it could happen that:

- the "intensive" version of the enzyme is already present in the eggs of the intensive females, so that it immediately exercises its function;

- in the eggs of the frosted females this enzyme is missing, when the allele arrives brought by the spermatozoon it begins to produce the protein in more advanced embryonic stages, starting to actually work a little later.

This explains why the offspring of intense females may be slightly higher in quality.

- the double intense has both phenomena, so it has a somewhat excessive phenotype;

-buffs from a regular coupling have the enzyme that works well, but not too much, because it is somehow (unknown mechanism) "attenuated" in the intensive parent, and produces regular feathers;

-the coupling between two buffs generates offspring in which this attenuation tends to get lost, so the feathers grow too much, like other skin productions. The loss of regulation could be gradual in generations.

Of course this is just an idea that should be demonstrated, but which once again highlights how complex the fascinating study of mutations in our feathered pets can be.

Editor's note: we inform you that this article was also published on the pages of Italia Ornitologica, in the number 8-9 of August-September 2018.

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