I've been trying to get a better grasp on the genetics of some of the morphs lately. I have done a lot of research and reading of some of the snake genetics books that have been produced recently. This has prompted me to do a lot of thinking and re-thinking (probably too much) about the morphs that are currently available. In doing this research/thinking, I ran across something that sparked a question in my mind. The notion of Allelic Mutations in the Cornsnake Morph Guide suggests there is a form of genetic mutation that interrupts the amount of Melanin produced. This interruption however does not cause the animal to become Amelanistic, rather it represents a change in the amount of melanin that can be produced by reducing it to some percentage other than zero (0%) as expressed in Amelanistic animals.

The Cornsnake guru’s have termed this form of mutation as “Ultra” which they suggest represents a shift in pigmentation (melanin production) to about 25% of the normal amount. They also state that animals are capable of producing more than 100% of the normal amount of melanin which would only be visually expressed as 100% or normal. They go further to express that the “Ultra” gene is paired at the same locus as the Amelanism gene and that an animal carrying the “Ultra” gene would be “Single Het” for both genes (“Ultra” and Amelanism). This means that the resulting offspring would be het for one gene or the other at the same locus and not het for both as a true double het animal would be. These animals would further be visually normal and you would not be able to tell which gene they actually carried. Personally, I wish they would have termed this as a “Di-het” in that the animal could be het for two genes at the same locus position. This may have simplified things for most if us.

The notion of “Ultra” is further expanded to say that an animal that inherits an “Ultra” gene from each of it’s parents would be 100% “Ultra” or have a pair of “Ultra” genes at the same locus position and they would produce roughly 50% of the normal amount of melanin. These animals would visibly be much lighter than either of it's parents. If one of these “Ultra” offspring were then plugged into a breeding trial with and Amelanistic animal, the resulting offspring would contain “Ultramel” and “Amelanistic” animals. They suggest that the Amelanistic animals would not be het for the “Ultra” gene since they would have inherited two Amelanistic genes at the same locus position (would not be carrying the “Ultra” gene). The other offspring (“Ultramel”) would have inherited an Amel gene and an “Ultra” gene and produce roughly 25% of the normal amount of melanin. These animals would be even more visibly lighter than the “Ultra” parents and also carry the paired gene for Amelanism (they would be het for Amelanism).

So why have I gone thru all the trouble of explaining the “Ultra” and “Ultramel” genetics that occur in Cornsnakes but have not been recognized in Boa Morphs? Or have they? Maybe the “Ultra” and “Ultramel” genetics are still too new to be recognized. Maybe they have just been identified as something else in the Boa community. With all of the questions that are running through my mind, the one that keeps coming back is my wondering if there is any difference between the mechanisms driving genetics in the different species of snakes. Can the mechanisms driving “Ultra” and “Ultramel” in cornsnakes be exactly the same, completely different or only slightly related in Boas? I think it can but I haven't seen any proof that it applies across the board.

If cornsnake and boa genetics (or even snake genetics in general for that matter) are that closely related, then my mind persists to question if it is possible that the Boawoman Caramel Hypo genetic mutation could actually be a precursor mutation (visual het) driving the “Ultra” genetic mutation (in this case the Paradigm Boa) or could it be the “Ultra” mutation in itself? If any of this is true, we may have simply overlooked the possibilities or just plain didn’t know what we were actually working with at that time. Regardless, the Paradigm Boa mutation could be the same the “Ultra” gene with even better mutations yet to come or it could be the same as the “Ultramel” genetic mutation with the next step being a full albino that is not capable of producing any hets for the Paradigm genetic mutation. If there are differences in the genetics, then it's also possible that an “Ultra” Boa gene may have some percentage other than the 25% it represents in cornsnakes which would mean that there are even more Paradigm Boa pigment variations on the horizon.

Since an “Ultra” form of genetic mutation exists which interrupts (reduces) melanin production, then couldn’t there also be a form of genetic mutation that exaggerates (increases) the amount of melanin production as well? And if it does exist, where would it be hidden? Could it be a “Tri-het” mutation (third possible mutation at the Amelanism locus). Could an exaggeration mutation be paired at some other point possibly with the Anerythristic gene locus or another locus point altogether? Maybe the real dark Peruvian Boa that was being offered for sale a few months back was this mutated gene.

Logically, it seems that the Caramel and Paradigm genetics hold the same functions as the Ultra and Ultramel genetics. I'm just looking for reasonable explanations.

Thanks,
Chris

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