Reptile & Amphibian Forums

i was thinking today about if co-dom visable morphs could be latent(not-visable) given certain circumstances. an example i was thinking about was
SuperPastel Lesser(male) * SuperPastel Lesser(female)...now the offsring would all(i believe) have to be super pastels, as well as lesers, however...if a super lesser(leucistic) was born, the pastel gene would be over-ridden and not visable (i assume). Therefore the all white luecistic would still technically be a super pastel as well and bred to a normal would produce all pastel lessers? any insight? thx

Not to make things confusing but there is more going on here than codominance. The Lesser Platinum along with a number of other mutations in likely to be a null mutation, haploinsufficient or hypermorphic mutation not codominant. If that is the case you are correct. You have the possibility of producing Super Pastels, Super Pastel Lessers and double homozygous Super Pastel-Super Lessers AKA Blue Eyed Leucistics. Because your parental stock were both Super Pastels you know that all of the offspring are Super Pastels, but due to the Super Lesser wiping out all of the pigment you are left with a phenotype of an all white snake. Now if your breeding pair was a Pastel Lesser and a Super Pastel Lesser you would not be able to visually distinguish the difference between Leucistics that are Super Pastels and the Leucistics that are Pastels.

Most breeders/hobbiests are unaware of any other forms of domianace besides dominance and codominance here are a few other possibilities.

Null Allele (Null Mutation)- A nonexpressed allele; a mutation that completely eliminates function of a gene. Mutation that abolish the function of a protein encoded by the wild type allele. Such mutations either prevent synthesis of the protein or promote synthesis of the protein incapable of carrying out any function.

Haploinsufficiency- A rare form of dominance in which an individual heterozygous for a wild type allele and a null allele shows an abnormal phenotype because the level of gene activity is not enough to produce a normal phenotype.

Hypermorphic Mutation- Produces an allele generating either more protein than the wild-type allele or the same amount of a more efficient protein. If excess protein activity alters phenotype, the hypermorphic allele is dominant.

To my knowledge the above mutations can only be identified by chemical testing, but what is happening with a number of ball python mutations dose not phenotypically fit the definition of codominance.

Hope this helps,
Greg

Graziani Reptiles

nt

Yes very helpful, thank you greg!

I believe the classical examples of codominance are haploinsuficiency examples as well due to a null mutation...

As with most science, there are almost no cases that actually fit with the classical examples...
I think most or many of the ball mutations thus far discovered alter things at the developmental stage. The mutations may not be in or around the genes affected at all, but rather in temporally expressed trans acting gene (such as a sigma factor, activator, repressor, etc...)

Super Cinnamons for example are patternless even before all of their pigment fills in. They also have slightly altered physical structure, which might be a function of more than a single gene. So, it seems possible that the cinnamon gene alters developement early on and broadly affects embryo development. Think about a mutant transcription factor that changes the production and ratio of multiple other genes...

However, the thing that is most interesting about balls scientifically is that there are very few systems that have been studied so well morphologically and yet almost nothing is known about the physiology. If only there was research money for this field...If there was a health angle to ball pythons, maybe the NIH would fund a study...
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when life hands you lemons, make super lemons, bumblebees, etc...

the fact that Co-Dominant is often misused. Most of the morphs thus far produced are incorrectly labled codom when they are more likely incomplete dominant. But since I didnt have my foot in the door 20 years ago to prevent improper coinage its highly unlikely everone will change their habits now.

Just my $0.02

Happy Breeding Everyone. Bring on those "co-dominants"!!!!!!!!!!

>i was thinking today about if co-dom visable morphs could be latent(not-visable) given certain circumstances.

Yes, indeed. There are two possible answers to this:

1. The genetic principle of epistasis, in which a mutant gene at one location in the genome masks the expression of a mutant gene at another location in the genome. For example, in mice, the albino mutant gene (a recessive mutant) can prevent the expression of the sombre mutant gene (a dominant mutant), which produces a nearly black mouse. An albino sombre mouse has the sombre gene and can pass it on to the offspring. But such a mouse looks just like an albino mouse that is normal at the sombre mutant's location in the genome.

Inheritance pattern of the mutants has nothing to do with epistasis. In other words, depending of what the mutants do, a dominant mutant can mask the presence of a dominant mutant, a codominant mutant or a recessive mutant. Or a codominant mutant can mask the presence of a dominant mutant, a codominant mutant or a recessive mutant. Or a recessive mutant can mask the presence of a dominant mutant, a codominant mutant or a recessive mutant.

2. The genetic principle of incomplete penetrance. In this, because of other genes or environmental factors, a dominant mutant simply is not physically manifested. For example, in a percentage of humans with the polydactyl (extra fingers) mutant gene, the person just has five fingers on each hand and five toes on each foot. Yet this person's children who inherit the mutant have six fingers/toes.

For both principles, the biochemistry has to be worked out individually for every example. And in most cases, the biochemistry has yet to be worked out, as far as I know.

Hope this helps.

Paul Hollander