Reptile & Amphibian Forums

What do you think a Axanthic Super Mojaves would look like...what small visual detailes do you think would differentiate them from Blue eyed lucy's?

ok ok yeah I know a white snake..but what small visual details could the Axanthic contribute that would stand out?

Kinda looking for people with experience producing combos with Axanthics or Mojaves, but any ideas are appriciated.

Thanks
-----
Becky & Crew
All Exotic Reptiles AKA WFReptiles

k
-----
Becky & Crew
All Exotic Reptiles AKA WFReptiles

Your asking how axanthicism would effect an already "all white" snake! If it were an Ivory, it would be a different story!

k, thanks.
-----
Becky & Crew
All Exotic Reptiles AKA WFReptiles

k, so what I am hearing is that you think once you get an all white snake, which a super mojave is not an all white snake ...your done?

You dont think you can tweek that at all.... maybe inhance colors, patterns, things that were hidden before, or add things to it that were never there...

I might be wrong.... but I think we need to think out of the box with the all white snakes. I dont think they are all "the end of the project"

I think theres some things to be done with them....I am hoping.

-----
Becky & Crew
All Exotic Reptiles AKA WFReptiles

Unfortunately, from a genetic standpoint, once you have a gene that removes something it's not usually possible to add it back. Take Albinism for example. Albinism removes black pigment (what's really happening is that Albinos are unable to produce the melanin that is responsible for black pigment). No matter what other genetic combos the Albino snake may possess, it will not have black pigment because it can't produce any.

Axanthism removes yellow pigment, so even though a Super Mojave may not be a true all white snake, if it doesn't have any yellow pigment to start with, then the only way to tell an Axanthic Super Mojave from a non-Axanthic Super Mojave will be through breeding.

Another example- I got my start in learning about genetics by breeding gerbils as a kid. Fortunately, there is quite a bit of information from a scientific standpoint on gerbil genetics because there is a Dutch university that has put a lot of effort into research so as far as color morphs go we know what alleles are present at each locus to cause a particular color trait. There is a trait in gerbils called Pink Eyed White. As you can imagine, it's a white gerbil with pink eyes. The Pink Eyed White trait is caused by the gene combination ** c(h)c(h) ** ** pp. For comparison, a normal (Wild Type/Agouti) gerbil would have the gene combination A* C* E* G* P* (the asteriks represent alleles that don't impact the appearance - a gerbil that carried recessive alleles might have the gene combination Aa Cc(h) Ee Gg Pp but it would look the same as a gerbil that was AA CC EE GG PP, or het for nothing). Basically, in the case of the Pink Eyed White gerbil, no matter what alleles are present at the other 3 loci, the gerbil will be white with pink eyes. For breeding purposes, it may still be a very useful animal because of the genes it carries, but the appearance doesn't change.

Hopefully that all makes sense...let me know if I need to clarify anything. It's kind of hard to explain without writing tons.

Thanks for all the info.
-----
Becky & Crew
All Exotic Reptiles AKA WFReptiles

A lot of info to go over, thank you. Gives me some things to think about.
I appriciate your time.
Becky
-----
Becky & Crew
All Exotic Reptiles AKA WFReptiles

The problem is the essential term: leucistic. A leucistic is missing the base gene for all pigment cell production OR the precursor protein for all pigments.

Therefore, adding in a morph gene that would modify pattern or colors would be subjugated by the leucism gene mutation. No matter what the additional morph gene codes for, it will be wiped clean by the leucistic gene(s), in theory, see below.

Now, this is also assuming that this term "leucistic" applies denotatively to the Blue and Black Eyed Lucies we often produce. This issue was discussed below with Anthony McCain's use of the term to describe a Mystic Potion (I think that's what it was...)
Not necessarily incorrect depending on whether you define leucistic as a genetic, phenotypic, or morph combination.

This is an ongoing problem with the entire "Hypo" complex of morphs as well. Is it truly hypomelanistic? Or is it erythristic, hyperxanthic, hypo-pigmented altogether, or something else?
-----
Lincoln, NE
0.1 Pastel, 1.0 Pastel het Pied, 0.1 Pied, 0.1 Cinn, 1.0 Black Pewter, 1.0 Woma (hidden gene?), 0.1 Yellowbelly
2.1 Normals, 1.0 Thayeri, 0.1 Thayeri X Alterna, 0.1 Whitesided P. catenifer sayi, 0.1 crazy cat, 1.0 husband

LOL...we were both posting at the same time

Sorry Bolitochrome, just wanted to add more specifics to your response.

Leucism is a Genetic mutation where the pigmentation cells in an animal fail to develop properly. This can result in unusual white patches appearing on the animal (piebald) or completely white creatures.

This is true depending on who you ask. Which makes it even more of a PITA.

A well respected geneticist printed a book several years back trying to pin down snake morphs. He defined leucism as a complete lack of pigment, leaving the eyes unaffected. By his definition only the Super Fire complex animals, Black Eyes Lucies, would be true Leucistic. This chap, by the way, has never worked with Ball Pythons or Boas, just native North American species.

This is the same definition held for fish and frogs, but not for birds and mammals. These latter creatures have piebald, calico, leucistic (sometimes even albino) all grouped into one category. This is probably because they often only have one or two pigment types, whereas Herps have at least 3.

Birds and mammals also have pigment cells that distribute from the neural crest of the embryo, almost always resulting in even distribution of pigment where it is darker on top with a lighter colored belly (we see this all the time). Herps have an array of genes that control pigment distribution, as we well know, which makes things even MORE complicated.

Anyways, here is a cool picture that got me interested in all of this. The pigment distributed from the neural crest of this bird's embryo on only one side.

Courtesy of Junglecats
-----
Lincoln, NE
0.1 Pastel, 1.0 Pastel het Pied, 0.1 Pied, 0.1 Cinn, 1.0 Black Pewter, 1.0 Woma (hidden gene?), 0.1 Yellowbelly
2.1 Normals, 1.0 Thayeri, 0.1 Thayeri X Alterna, 0.1 Whitesided P. catenifer sayi, 0.1 crazy cat, 1.0 husband

The definition I gave for leucism doesn't change no matter who you are or what you may think. That is what leucism is.
leucism is also the same for all creatures and is completely different from albinism, which are not the same thing. Albinism is lacking melanin, while leucism affects all color pigments.
Leucism like you said is believed to stem from the the mutated cells in the neural crest, which is why it doesn't affect the eye color. I tend to disagree with this a little because blue or red irises are not normal BP eye colors.
Super fires have a high tendency to be pied looking BEL's.

Again, I will say, this isn't my opinion. It is what is in the literature. The definition tends to change with taxa because the genetics causing reduced pigment are not well understood.

"The definition I gave for leucism doesn't change no matter who you are or what you may think. That is what leucism is. Leucism is also the same for all creatures..."
Not what my ornithology textbook taught. Also, fish albinism and leucism are more often than not considered the same thing. Again, in the literature. Not my opinion or interpretation. This what other scientists are publishing and teaching. I agree it is largely incorrect or incomplete.

In any case, it is a moot point.

If possible, it would be ideal to fund genetic and phenotypic studies of Ball Pythons to develop, for our own purposes, our own definition of leucism (as well as hypomelanism, xanthic, iridic, piebald and establish patterns of chimerism while we are at it).
-----
Lincoln, NE
0.1 Pastel, 1.0 Pastel het Pied, 0.1 Pied, 0.1 Cinn, 1.0 Black Pewter, 1.0 Woma (hidden gene?), 0.1 Yellowbelly
2.1 Normals, 1.0 Thayeri, 0.1 Thayeri X Alterna, 0.1 Whitesided P. catenifer sayi, 0.1 crazy cat, 1.0 husband

Would be very nice for some studies to be done to actually clarify things and put everyone on the same track.

Just found this which says we are both wrong. It also shows how much we don't know and how much people think they know, which is actually/factually wrong.

This article is very informative.

Here is the link to the full article:
Leukism(leucism)

here is an excerpt:

LEUKISM (LEUCISM)- medically defined this is a defect in the skin, not the pigment cells. There are other derangements of pigment that can cause a whitening effect, but they are not classical leukism. Classical leukism is caused by a faulty gene, or set of genes, that causes the skin to be unable to support pigment cells. Experiments have been done that illustrate this. In one set of experiments normal pigment cells from a normal animal were placed in albino skin and the cells were normal and produced pigment. This demonstrated that the albino defect was in the pigment cells of the albino but not in the skin itself. The same experiment done in leukistic skin caused the normal pigment cells to die. Some have claimed that the reason eyes are pigmented in leukistic animals is because the pigment in the eye comes from another origin (the non-neural crest theory). This is really not the case. In fact some (unfortunately as yet unpublished research that really needs to get published) experiments were done transplanting RPE eye pigment cells into the skin and they died. Conclusion? Well nothing. The eye pigment cells can't survive out of the eye is all that proved. So melanophores from the iris were transplanted and they died in leukistic skin but survived in albino skin. Conclusion? The defect has to do with the skin, not the origin of the pigment cells. Further evidence of this can be found in numerous species that have melanin or other pigments present in other tissues such as the peritoneum but are typical of leukistic animals on the outside when alive.

However, some leukistic animals are also leukistic internally. What does this mean? At present it is unknown. It might reflect a subtype of leukism where there is agenesis, dysgenesis or complete necrosis embryologically of the chromatophores. This could represent another branch on the leukism scheme and might indicate a disorder we might call Complete Leukism. Where forms just limited to the skin might be termed Cutaneous Leukism. One thing is clear, the definition of leukism is only semi set. There is room for other forms, but it should be understood that there must be a standard definition defined in pathological terms.

So are there other forms of leukism? Possibly, but one must not confuse leukism with dysregulation of dysfunction of chromatophores. For example, if the chormatophore cannot produce pigments, but is otherwise functional, that is albinism. However, what about a mutation in a receptor that causes the pigment cell to be unable to receive signals (a MSH receptor for example) to produce pigment? That situation is more closely related to albinism since the pigment cells are present but not functioning, though they are dysfunctional from a different cause. Thus it is probably better call the condition something else in order to eliminate confusion. I personally refer to these potential disorders as receptor mediated chromatophoropathies (or chromatopathy) or RMC's. I first coined the term RMC back in 2003, but have had no real case where this could be proven. Since many of the immunohistochemical markers for mammal receptors do not work in reptiles and leukistic or RMC mammals are much harder to come by, I have not been able to publish the term in the mainstream literature. But published or not, it is useful for this discussion.

I have also seen, but could not prove, another condition. A client of a colleague has a snake that went white like a "snow corn" over a few months. It suddenly died. Upon necropsy there was a tumor in the brain. I suspect, but without immunohistochemistry that would work on reptiles could not prove that the MSH producing cells were destroyed by the tumor. Because of this case I had to also add another possible disorder. Whether acquired or through genetic mutation, a deficiency in the hormone stimulating the chromatophores is possible. I refer to this possible disease as Hormone Mediated Pesudoalbinism or Pesudoleukism. In the case I described, my colleague failed to notice if the eyes retained any pigment, so I am not sure what the presentation would be. But with all the confusion these classifications can separate some of the confusion like this:

1.
Classic leukism is due to chromatophore necrosis, apoptosis, dysgenesis or agenesis - and is the the absence of recognizable chromatophore cells on histopathology.
2.
Receptor Mediated Chromatophoropathy (RMC) is a white state due to chromatophores not receiving signals or are receiving only low level signals to produce pigment due to a mutation in some receptor or signaling pathway, but chromatophores are present in the skin on histopathology.
3.
Hormone Mediated Pseudoalbinism or Pseudoleukism (HMP complex) is a white state due to a deficiency of stimulatory hormone, but the chromatophores are present in the skin on histopathology. In this case the chromatophores are completely normal. They are reacting normally to an abnormal condition (lack of stimulatory hormone), so they are neither leukistic, nor albino. The appearance of these animals might mimic leukism or albinism.
4.
Albinism is a defect of pigment production within the chromatophores without loss of chromatophores. Chromatophores are present in the skin, but are not able to produce pigment or fully formed pigment.

Yes, I have read this article. Though I agree with this individual, the problem continues that a variety of other, equally respected scientists used several different definitions of leucism. I would certainly vote for making this the be-all, end-all resource for our own definitive purposes though.

Here is the book I referenced before. His grouping of "calico" and piebald animals is interesting:

"Reptile and Amphibian Variants: Color, Patterns and Scales" by H. Bernard Bechtel, 1995.
-----
Lincoln, NE
0.1 Pastel, 1.0 Pastel het Pied, 0.1 Pied, 0.1 Cinn, 1.0 Black Pewter, 1.0 Woma (hidden gene?), 0.1 Yellowbelly
2.1 Normals, 1.0 Thayeri, 0.1 Thayeri X Alterna, 0.1 Whitesided P. catenifer sayi, 0.1 crazy cat, 1.0 husband