Can Certain Variations of Dominant Morphs Effect how many Supers?

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Originally Posted by RandyRemington

The definition of a dominant mutation is one where the heterozygous mutant and homozygous mutants are the same non wild type phenotype. Pinstripe is the only proven dominant ball python morph I'm aware of. BHB reports having a proven homozygous pinstripe that looks like a regular (heterozygous) pinstripe but produces 100% pinstripe offspring.

If homozygous spiders don't hatch that would qualify spider as being technically co-dominant because the homozygous mutants are different (dead) than the heterozygous visible mutants. A homozygous animal surviving to breeding is actually needed to prove if a mutation is dominant.

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Congo is the other proven dominant gene and there is no proof that homozygous spider die....

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Originally Posted by RandyRemington

If homozygous spiders don't hatch that would qualify spider as being technically co-dominant because the homozygous mutants are different (dead) than the heterozygous visible mutants. A homozygous animal surviving to breeding is actually needed to prove if a mutation is dominant.

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You know, I would've said the same thing, but I think that isn't correct. Achondroplastic dwarfism in man has a homozygous lethal form, but it is considered dominant, not co-dominant. I think that other homozygous lethal traits are as well.

I think that your working definition (which is the same as the one in my head as well) is actually incorrect. Spider and achondroplasia are dominant because the mutant phenotype is dominant over the wild-type phenotype in the heterozygous form, regardless of what happens in the homozygous form (a dead/unformed versus indistinguishable homozygote).

In the case of the morphs we call co-dominant, which should really be incomplete dominant, there is actually a blending of the "pure" homozygous mutant and the pure wild-type form. Super pastels are the "pure" homozygous mutant, for example, and the regular pastel is a "blending" of that plus the wild-type. The reason we say we have to wait and find out if there's a "super" form or not before we label a mutation co-dom or dom is to find out whether a given heterozygote that we're looking at is actually the less-extreme, "blended" version of a "pure" homozygous mutant phenotype (which is invariably more extreme than the heterozygote in that case). Does that make sense? That was a run-on sentence and I might've just confused myself ...

I guess because you can't "blend" the lethal form (because it's a phenotype that essentially doesn't exist since it's incompatible with life) and the wild-type, you just consider a homozygous lethal mutation to be simple dominant ... :confused:

(Co-dominant, BTW, is where BOTH traits are expressed equally ... AFAIK there aren't any traits in ball pythons that could be truly considered co-dominant, and most of the true co-dominant traits I know of are expressed on a microscopic level ...)

Honestly it's all just semantics. I think a lot of these terms are pretty out-dated when you talk to geneticists ... :P (They are wicked useful, tho ...)

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Originally Posted by OhhWatALoser

there is no proof that homozygous spider die....

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I agree that a complete lack of a homozygous spider isn't proof that the trait is homozygous lethal.

However, with the spider morph's popularity, a complete lack of a living homozygous spider is pretty weird, don'cha think?

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Originally Posted by mainbutter

I agree that a complete lack of a homozygous spider isn't proof that the trait is homozygous lethal.

However, with the spider morph's popularity, a complete lack of a living homozygous spider is pretty weird, don'cha think?

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well with the pinstripes popularity and there only 1 known homozygous, its hard to prove out homozygous dominant genes. I know NERD said they did enough breeding to prove it dominant, but I don't know exactly how hard they tired to prove homozygous, but Kevin said he doesn't think one exists. I just wish we had the data lol.

If one wild type copy of a homozygous lethal mutation can keep the animal alive wouldn't that count as a blend? At least with HG Woma we get to see that the pearl phenotype is different before it dies (with the one possible recent exception). Maybe a homozygous spider would look different if we got to see it?

As far as proof of a homozygous spider goes, I would say there is no proof that they live. The safest assumption might be that no new genotype can survive and breed until proven given that it might be impossible to prove if they don’t.

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Originally Posted by RandyRemington

If one wild type copy of a homozygous lethal mutation can keep the animal alive wouldn't that count as a blend? At least with HG Woma we get to see that the pearl phenotype is different before it dies (with the one possible recent exception). Maybe a homozygous spider would look different if we got to see it?

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I honestly don't know where the line is drawn in terms of semantics (incomplete dom versus dominant) for lethal genes. I think a lot of it is just convention, because we're finding it more and more difficult to fit the complex "round pegs" of molecular genetics into the "square holes" of the simple Mendelian classifications systems.

In my mind, I could justify the semantic classification that a homozygous lethal gene that kills the neonate after birth (like the pearl) could be considered to be incomplete dominant, whereas one that was incompatible with life and did not allow the embryo to form very far past fertilization could be potentially considered simple dominant (since there is no homozygous "phenotype" to compare it to, it's just a nonexistent entity). Really though, I think that's kinda stretching it and I'm just trying to justify the nomenclature as I've seen it used. :P (I have also seen suggestions that we may classify different pleiotropic effects of the same gene differently; for example, we could classify the pattern part of the woma gene as incomplete dominant and the lethal neurologic part as simple recessive, even though they're assumed to be the same gene. Confusing!)

BTW, in looking this up and doing more research into the lethal white foal syndrome, evidently that was a bad example for a simple homozygous lethal trait -- apparently, there is huge debate as to how it is linked to the overo coat pattern, and whether it's even a pleiotropic effect of the overo gene at all. There's also a lot of politics involved, apparently ... Guess we shouldn't feel so bad about all the confusion surrounding the mutations we work with -- I'd say that we're not doing so bad trying to figure it out on our own (ie, without any research or funding for it!)