Hello Chris,

First let me say...I am by no means a genetics guy...but I do find it interesting....

I did not know where to put this post but hoped you would see it here.....

I have been thinking about Celia's Hypo/Motley litter....

Everyone says that the Hypo trait plays games with other traits causing great confusion....
I have seen hypo Arabesques...that I really did not think were Arabesques.....but they were...I guess....

My Theory for what is going on is that when the two co-dom traits come together...one tries to dominate the other and in my opinion the hypo trait is the Victor in most cases.

This makes sense to me...except that in Celia's litter...the normals were affected as well. But I found some reading that seems to make it sound like a new form is created...please read below....


My theory:

If this genetic crossover plays havoc with the melanin....and the Motley being mainly a form high in melanin...that if the melanin was shut off genetically would not the hypos take on a super hypo form? Now would this animal still reproduce both forms??

The following is just pasted in from something I found....

Gene Function and mutant alleles


It is important to realise that almost all colour morphs are produced by defective alleles for a locus pre-existing and functional in the normal bird. All these new colours are not being produced by the new mutant allele, they are being revealed by the dysfunction caused by the allele. Once this fact is realised, we can start to view colour morphs in a new light and begin to understand the true action of each locus that they help us identify. It is what is missing from the wildtype phenotype that is the true product of the locus being investigated.

If the mutant alleles for a locus are recessive to wildtype, then that tells us that a single functional wildtype allele is all that is needed to produce the gene product. If mutant alleles are co-dominant or dominant, then we know that the gene product requires two functional alleles coding for it, to produce its full effect. This generally indicates that the gene product is a protein with at least two base units (a dimer).

Co-dominant interactions can produce the third phenotype in three different ways. The most common is a blended type. In this case the heterozygous phenotype is midway between the two homozygous phenotypes. The best example is the dark factor locus where one mutant allele results in half the function of the homozygous wildtype genotype and two mutant alleles result in virtually no function. Alternatively, in cases where alleles have differential expression in different parts of the plumage, the heterozygous form is a sum of the greater effects. This is seen with the dilute locus in Budgerigars, where different alleles differentially deposit melanin within either the cortex or the medulla and the heterozygous phenotype represents a combination of the greater effects of each allele.

The third type of co-dominant interaction is known to occur only with alleles of the blue locus. It involves the process of complementation. In these cases the gene products of certain heterozygous genotypes are more functional than either mutant allele normally would be alone. The most likely theory is that the defect from different alleles act in a complementary interaction with one another, resulting in a greater than expected enzyme function for the end product.

As more colour morphs are discovered in each species, multiple allelic series are becoming increasingly identified. This is to be expected because there is a limited number of loci involved with pigment control and therefore limited places where a mutation can occur. So far no allelic series is known for loci with dominant or co-dominant mutant alleles, only those with recessive mutant alleles. And in all known cases a dominance hierarchy is formed within the allelic series. Mutant alleles with greater function (closer to wildtype) are either dominant or co-dominant with alleles with less function. I know of no situation where less functional alleles are dominant to other alleles in a series.


Andy
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