Mark Dwight
New member
I've been doing some research lately on pigments of reptiles and amphibians and think I may have stumbled on why lavender cornsnakes are so much different than any other color mutants of cornsnakes. This is just a theory but I think I may be on to something. But in order for me to explain it I'll first need to give a little lesson on reptile pigments. I'll do my best to keep it as simple as I can so as not to bore you to death with all the fine details...only the bare bone basics.
So here go's..
Almost all of the colors we see in snakes come from color bearing cells called
Chromatophores. There are three sub-classes of chromatophores in snakes. 1. Xanthophores, 2. Melanophores and 3. Iridophores. These three types of
chromatophores have different pigment functions. The Xanthophores produce the yellow to red pigments. And the Melanophores produce the brown and black pigments. And the iridophores react with xanthophores and melanophores to reflect other hues of color(like green and blue.) The xanthophores and iridophores reside in the dermis layer of the skin just beneath the epidermis. The melanophores can be in both the dermis and epidermis. The epidermis is a layer of about 30 dead skin cells deep on top of the living dermis layer. The Chromatophores are also arranged in layers. The top layer contains the Xanthophores, in the middle are the iridophores and the bottom layer is the Melanophores. The Melanophores also have finger like projections called dendrites that can extent upward between and
around the iridophores and Xanthophores. The Melanophores can send melanin (the brown or black pigment) through these dendrites to the surface of the dermis and into the epidermis partially covering up the pigment produced by the Xanthophores. This is why some snakes like Boa constrictors can quickly change from light to dark.
OK. Now that we've gotten that out of the way.....
If you've ever seen a baby snake that was born or hatched prematurely you may have noticed it had a lot less pigment compared to a fully developed baby. Thats because all of the chromophores had not yet migrated from the neural crest to the dermis of the skin. Early in the embryonic development of snakes the cells that will eventually become the chromophores are being created in a region called the neural crest. I like to think of the neural crest as a cell nursery. At different points in development these cell leave their neural crest home in waves and seek out other parts of the developing
embryo. The waves of pigment cells leaving the neural crest and migrating to the dermis are called chromatoblasts. But sometimes things go wrong and there is a defective mutant gene that will not allow chromatophores to develop in the neural crest or the defective gene will prevent the migration of the chromatoblasts to the dermis. Either way no chromatophores ever reach the dermis. This condition is called leucism. Leucistic snakes have no melanophores, no xanthophores and only very limited amounts of iridophores and their skin appears completely white. However, eyes get most their pigment from cells that migrate from a region called the neural tube and not the neural crest. So the eyes are affected very little by the leucistic mutant gene. Leucism can be classed as a genetic malfunction of the neural crest.
So what does this have to do with lavenders?
The phenotype of a homozygous lav is a reduction of all common cornsnake pigments like red, orange, yellow, black and browns. Now I asked myself how
could a singe recessive gene possibly be limiting the production of melanin
(needed to make black and brown color), pteridine (needed to make yellow pigments), and carotenoid (needed to make red and orange pigment.) I find
it hard to believe a singe gene could control so many chemical actions. And
that's because it DOESN'T! I believe that like the leucistic gene the
lavender gene is reducing the amount of pigment bearing chromatophores from reaching the skin. The lavender gene is a malfunction of the
neural crest. Unlike the leucistic gene however some chromatophores do
reach their destination. Kind of a wanna-bee leucistic.
Keep in mind this is just a theory. But from what I know about pigments, cell migration and genetics it does make sense to me.
Oh btw this theory also explains their light purplish/brownish color. It also explains why lavenders will partly "mask" all other color mutants like caramel and anery. With limited chromatophores lavenders are changed very slightly when another color mutant is added to the mix.
I'm a boa breeder as well as a corn keeper. I once had a litter of boas that were born only about half way through their gestation period. I can remember thinking to myself that in color those babies looked just like lavender corns. The more I think about this theory the more I like it. It may also explain some of the strange things we see going on in other color morphs(like melanan masking the red in aneryA's and yellow masking the reds in caramels, but I'll leave that story for another post.)
So here go's..
Almost all of the colors we see in snakes come from color bearing cells called
Chromatophores. There are three sub-classes of chromatophores in snakes. 1. Xanthophores, 2. Melanophores and 3. Iridophores. These three types of
chromatophores have different pigment functions. The Xanthophores produce the yellow to red pigments. And the Melanophores produce the brown and black pigments. And the iridophores react with xanthophores and melanophores to reflect other hues of color(like green and blue.) The xanthophores and iridophores reside in the dermis layer of the skin just beneath the epidermis. The melanophores can be in both the dermis and epidermis. The epidermis is a layer of about 30 dead skin cells deep on top of the living dermis layer. The Chromatophores are also arranged in layers. The top layer contains the Xanthophores, in the middle are the iridophores and the bottom layer is the Melanophores. The Melanophores also have finger like projections called dendrites that can extent upward between and
around the iridophores and Xanthophores. The Melanophores can send melanin (the brown or black pigment) through these dendrites to the surface of the dermis and into the epidermis partially covering up the pigment produced by the Xanthophores. This is why some snakes like Boa constrictors can quickly change from light to dark.
OK. Now that we've gotten that out of the way.....
If you've ever seen a baby snake that was born or hatched prematurely you may have noticed it had a lot less pigment compared to a fully developed baby. Thats because all of the chromophores had not yet migrated from the neural crest to the dermis of the skin. Early in the embryonic development of snakes the cells that will eventually become the chromophores are being created in a region called the neural crest. I like to think of the neural crest as a cell nursery. At different points in development these cell leave their neural crest home in waves and seek out other parts of the developing
embryo. The waves of pigment cells leaving the neural crest and migrating to the dermis are called chromatoblasts. But sometimes things go wrong and there is a defective mutant gene that will not allow chromatophores to develop in the neural crest or the defective gene will prevent the migration of the chromatoblasts to the dermis. Either way no chromatophores ever reach the dermis. This condition is called leucism. Leucistic snakes have no melanophores, no xanthophores and only very limited amounts of iridophores and their skin appears completely white. However, eyes get most their pigment from cells that migrate from a region called the neural tube and not the neural crest. So the eyes are affected very little by the leucistic mutant gene. Leucism can be classed as a genetic malfunction of the neural crest.
So what does this have to do with lavenders?
The phenotype of a homozygous lav is a reduction of all common cornsnake pigments like red, orange, yellow, black and browns. Now I asked myself how
could a singe recessive gene possibly be limiting the production of melanin
(needed to make black and brown color), pteridine (needed to make yellow pigments), and carotenoid (needed to make red and orange pigment.) I find
it hard to believe a singe gene could control so many chemical actions. And
that's because it DOESN'T! I believe that like the leucistic gene the
lavender gene is reducing the amount of pigment bearing chromatophores from reaching the skin. The lavender gene is a malfunction of the
neural crest. Unlike the leucistic gene however some chromatophores do
reach their destination. Kind of a wanna-bee leucistic.
Keep in mind this is just a theory. But from what I know about pigments, cell migration and genetics it does make sense to me.
Oh btw this theory also explains their light purplish/brownish color. It also explains why lavenders will partly "mask" all other color mutants like caramel and anery. With limited chromatophores lavenders are changed very slightly when another color mutant is added to the mix.
I'm a boa breeder as well as a corn keeper. I once had a litter of boas that were born only about half way through their gestation period. I can remember thinking to myself that in color those babies looked just like lavender corns. The more I think about this theory the more I like it. It may also explain some of the strange things we see going on in other color morphs(like melanan masking the red in aneryA's and yellow masking the reds in caramels, but I'll leave that story for another post.)