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I don't know if it's just me, but I find it difficult to find resources that help me understand genes that are allelic on a fundamental level. I understand the outcomes, but don't understand the "why" if that makes any se[/b]nse.
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I'd agree, I also am fuzzy on the mechanics of Hypo/Strawberry and especially Motley/Stripe, doesn't help with the motley/stripe that the details I first learned about it are wrong but I've not heard a good description of the actual way it works, so only remember the not quite accurate first bit.
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Yeah, allelism can be a difficult concept to grasp, it is in the tutorial I'm working on but shows up after I explain a lot of other concepts that are helpful in grasping it. But I'll try to do so briefly here.
I think ultra and amel provide a good example. The amelanistic locus is on chromosome 3 of the corn snake. The exact gene responsible hasn't been identified but has been narrowed down to two candidate genes, both of which encode proteins involved in the synthesis of melanin from tyrosine. So the wild type allele at the amelanistic locus encodes the normal protein that carries out this function.
As you probably already know, all corn snakes have two copies of each (non sex) chromosome. So they have two copies of chromosome 3 and thus have two copies of the amel locus. The different variants of the amel gene (genes are often named after the first mutation described in them, which can get confusing) that can occupy the locus are called alleles. In corns, there are 3 known alleles of the amel gene: the wild type allele, the ultra allele, and the amel allele. So an individual corn can have two wt alleles, one wt one ultra, one wt one amel, two ultra, two amel, or one ultra one amel (ultramel).
Because the amel mutation is recessive to wt and homozygous amel animals (homozygous means both alleles are of the same type, in this case the mutant amel allele) produce no melanin, the amel mutation is assumed to be a mutation that completely inactivates the gene or its protein product. The reason that animals with one wt allele and one amel allele look normal is because the wt allele produces enough functional protein product to result in the synthesis of normal amounts of melanin, even though corns carrying one wt allele and one amel allele are predicted to make half as much functional gene product as homozygous wt animals.
This is probably because the enzyme encoded by the wt allele is not the rate-limiting step of producing melanin. For example, if you are trying to make ham sandwiches and you have 80 slices of bread and 20 slices of ham, you can make 20 sandwiches with 40 pieces of bread left over. So the ham is the "limiting reagent" in this case. So by dropping the number of bread slices to 40, you can still make the same number of sandwiches. In that analogy, the wt amel gene product is like the bread and the sandwiches are the melanin. For the sake of our analogy, assume each wt allele contributes 40 slices of bread and you need 20 sandwiches to have a wt appearance. In this instance, one wt allele and one amel allele is still sufficient to produce the requisite 20 sandwiches because there are still 40 pieces of bread. In our analogy, dropping below this threshold of 20 sandwiches would be expected to result in a mutant phenotype.
Like the amel allele, the ultra allele is also recessive to wt. However, it is incomplete dominant to amel. Ultramel animals have an appearance intermediate between wt and amel. This can be explained if the ultra mutation impairs the function of the melanin-synthesizing protein, but does not eliminate its function. Thus, an animal that has one wt allele and one ultra allele will look like a normal for the same reasons that het amel corns look normal.
A corn snake that has one ultra allele and one amel allele has a phenotype intermediate between normal and homozygous amel because it is still able to produce some melanin, but the amount produced is less than that produced by an animal that has one wt allele and one amel allele, or one wt allele and one ultra allele. In our bread analogy, a wt allele resulted in 40 bread slices, so imagine the ultra allele is comparable to 20 bread slices. An amel allele is zero bread slices. So an ultramel animal is producing 20 bread slices, but with 20 slices of ham that results in only 10 sandwiches. This drops us below the threshold of 20 sandwiches produced when at least one wt allele is present, resulting in a visible difference.
My prediction about the motley locus is similar. I suspect that the motley allele retains partial function whereas the stripe allele is completely nonfunctional. Some motley animals do have a stripe appearance, perhaps because of the combined influence of other alleles of different genes. People have said that animals with one motley allele and one stripe allele cannot be reliably distinguished from motleys, but it wouldn't be surprising to me if "motley stripes" were, if everying else is equal, more likely to have a pinstripe or stripe appearance than a regular motley, since they are predicted to have less functional gene product than a homozygous motley.
I hope that this is helpful, or at least a good starting point.
I seem to be leaning more towards evolutionary biology or vet school these days anyway, but I'm still open to ideas.
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