Reptile & Amphibian Forums

What is it that makes the anery gene do what it does.... specifically?

What switch is turned off, or rather what is the root source of the switch being turned off?

In albinism/amelanism it is a disruption or break in the tyrosinase enzymes function, ultimately diminishing or completely stopping melanin production by various means.

Does the tyrosine protein or tyrosinase enzyme have any effect on the production of xanthophores and erythrophores?

I have researched it until I am blue in the face. I hope that someone around here can help.

The more technical an answer, the better! Thanks!

-----
"Continuing to cling to the patterns you know, inhibits your ability to discover what you don't know." - Eric Allenbaugh

""What switch is turned off, or rather what is the root source of the switch being
turned off?""

Depends on the particular anerythristic gene(s) at work. Red pigment in reptiles
comes from carotenoids which must be metabolized from their diet. The carotenoid is
then transported to the erythrophores. There are many ways this system can break
down leaving no red pigment in the phenotype. For example a gene may simply not
allow the metabolism of carotene into carotenoids. Or a gene may halt the transfer
of carotenoid to the cell. Or a gene may not allow the carotenoid to migrate to the
cell walls. And still another way is that the pigment cells are not able to migrate
from the neural crest to the dermis of the skin. In all these cases the snake will
show no red pigment. But I haven't a clue which one of these
processes causes type 1 and type 2 anery in boas.

""In albinism/amelanism it is a disruption or break in the tyrosinase enzymes
function, ultimately diminishing or completely stopping melanin production by
various means. Does the tyrosine protein or tyrosinase enzyme have any effect on the
production of xanthophores and
erythrophores?""

No. The tyronsinase process is only found in the chromatophores called melanophores
which are responsible for the brown and black pigment in reptiles. This is
completely separate from the carotenoid and pteridine (yellow) process found in
erythrophores and xanthophores.

>What is it that makes the anery gene do what it does.... specifically?

Nobody knows.

>What switch is turned off, or rather what is the root source of the switch being turned off?

Nobody knows.

>In albinism/amelanism it is a disruption or break in the tyrosinase enzymes function, ultimately diminishing or completely stopping melanin production by various means.

Actually, nobody knows what causes abinism in boa constrictors, yet. Probably a malfunctioning tyrosinase causes either Sharp albino or Kahl albino, but nobody has tested for tyrosinase in either, so nobody knows for sure which it is. It is very unlikely that both are produced by a malfunctioning tyrosinase. And possibly neither Sharp nor Kahl albino is produced by a malfunctioning tyrosinase.

Caramel albino sounds to me like the mutant pinkeyed dilute in mice. Pinkeyed dilute is believed to be caused by a malfuction somewhere in the biochemical system regulating tyrosinase production/breakdown rather than in the gene actually coding for tyrosinase. But your guess is as good as mine as to whether that is the cause of caramel albino, too.

>Does the tyrosine protein or tyrosinase enzyme have any effect on the production of xanthophores and erythrophores?

As far as I know, no. The salmon (AKA hypo) mutant seems to increase yellow pigmentation while decreasing black pigmentation, but nobody knows what the mechanism is. The breakdown is probably somewhere other than in the tyrosinase enzyme.

Paul Hollander

-----
"Continuing to cling to the patterns you know, inhibits your ability to discover what you don't know." - Eric Allenbaugh