Here is a paper that I found in my research on the subject that I thought you both would be interested in. I wish I could remember the website I downloaded it from because I would really like to get in contact with this person. I have copied it in it's entirity. From what I gather from reading this paper, leucism (like albinism) is a genetic defect that is recessive. Because it is recessive, two leucistics bred together will produce normal/colored offspring who carry the leucistic gene (just like two albino's).
Here is is:
Color Anomalies in Snakes
by Myia Sindelar
Why are snakes called albino when they have obvious coloration? How does a pairing of two albino snakes produce normal offspring? What is the difference between leucistic and albino? The answers to these questions involve basic genetics and knowledge about skin pigment cells and the role they play in determining phenotype (outward appearance). While I in no way claim to know all about this subject, I have recently had the opportunity to learn some of the basics behind skin color aberrations in snakes (Actually Eileen forced (ha-ha) me to write a paper for her developmental biology class on the subject). The following paragraphs represent my feeble attempt to explain what I have learned.
Before I get into pigmentation, I thought it might be helpful to do a little background on the skin, where it comes from and what its function is. The simplest definition of skin is that it is a protective barrier between delicate body organs and the environment. The skin also prevents dehydration and protects the snake from toxic substances. Two other functions of the skin rely on the presence of melanin, they are protection from ultraviolet radiation and thermoregulation. The skin of a snake (or any vertebrate for that matter) is composed of two basic layers called the epidermis, the outermost layer, and the dermis, the underlying layer. The origins of these layers can be seen in embryonic development when cells differentiate into ectoderm, mesoderm and endoderm. The ectoderm will give rise to the epidermis along with skin glands and the nervous system. The dermis on the other hand will be formed from mesoderm along with muscles, bones, and the circulatory system. Lastly, endoderm gives rise to several organs and the lining of the respiratory and digestive systems.
Now for the interesting stuff. Skin color is determined by skin pigment cells called chromatophores. Chromatophores arise from the neural crest, a part of the embryonic ectoderm. Early in development these cells migrate to the skin where they may differentiate into one of three chromatophore types. These three types are melanophores, xanthophores and iridophores (this is where I consider reptiles lucky because warm-blooded creatures have only one type of chromatophore, the melanocyte).
Melanophores are cells responsible for synthesizing black and brown pigments. A process called melanosynthesis is essential to the production of melanin. Melanosynthesis involves the conversion of the amino acid tyrosine to melanin which is a somewhat complicated process that has two crucial steps. In step one tyrosine is converted to dihydroxyphenylalinine (dopa); step two converts dopa to dopaquinone. The key to these two steps is that it cannot occur without the enzyme tyrosinase. If tyrosinase is absent, tyrosine cannot be converted to melanin.
Xanthophores are pigment cells responsible for yellow, red, or a mixture of the two colors. The exact color of a xanthophore is determined by the number and combination of the yellow and red pigments in the cell.
Iridophores do not synthesize pigments, they do however produce color based on their physical properties. These cells house organelles called reflecting platelets that reflect and scatter light. The colors that can result from these cells are greens, blues, reds and browns.
These three cell types are situated in the epidermis and it seems that their location is predetermined by genes, although the exact mechanism is not fully understood. The density, distribution, quantity and quality of the pigment cells interact with each other to produce the colors and patterns we see. Pattern is more attributed to the melanophores and xanthophores and color quality is a result of the iridophores.
Variations from normal color and pattern occur for a number of reasons. The most common aberrancies are albinism, axanthism, leucism, piebaldism, and melanism. This is where the terminology can be confusing and misleading. To be perfectly honest, I am still trying to differentiate them in my mind as I write this. The best way to discuss these anomalies is to treat each one separately.
Albino as defined by Bechtel (1995) is a congenital (occurring from or before birth) decrease or absence of melanin in the skin, mucosa, and eyes. This is usually a result from an inherited defect in melanin formation. Mutations at various loci involving pigmentation can cause albinism or in simpler terms, more than one type of defect can result in an albino organism. The two most common forms of albinism are tyrosinase-negative albinism and tyrosinase-positive albinism. In tyrosinase-negative albinism, the organism is unable to synthesize tyrosinase, the enzyme necessary to convert tyrosine to melanin. This is the result when a homozygous recessive pairing of the gene controlling synthesis of tyrosinase occurs. Tyrosinase-positive individuals have the ability to synthesize tyrosinase but are unable to produce melanin for either or both of two reasons. The first reason is that although tyrosinase is present, tyrosine is not transmitted to the melanophore for conversion to melanin. The other reason is that tyrosinase inhibitors could prevent synthesis of melanin. Tyrosinase-negative and tyrosinase-positive albinos look the same, that is they have the same phenotype. Keep in mind that their genotypes are different. This is the reason why a cross between two albino specimens can result in all or some normal offspring. The following examples may be an easy way to understand this concept:
Assume a male with tyrosinase-negative albinism with the genotype (actual gene make-up) nnPP. The lowercase n represents the recessive mutation for tyrosinase-negative albinism. Assume a female with tyrosinase-positive albinism with genotype NNpp. The lowercase p represents the recessive mutation for tyrosinase-positive albinism. Using a simple Punnett square analysis we can expect the genotype of all offspring to be NnPp. All offspring would be heterozygous and their phenotype would therefore be normal.
Assume a male with tyrosinase-negative albinism heterozygous for tyrosinase-positive albinism with genotype nnPp. Assume a female with tyrosinase-positive albinism heterozygous for tyrosinase-negative albinism with genotype Nnpp. A cross between these two snake would result in the following genotypic frequencies: NnPp:nnPp:Nnpp:nnpp. These genotypes would result in the following phenotypic frequency: 1 normal:3 albino.
The last aspect to mention concerning albinism is that it only affects melanin production. Xanthophores in an albino snake are functional and are still capable of producing pigment. This is why some technically albino snakes have yellowish or reddish coloration. Axanthism is a term that was unfamiliar to me until I researched this topic. Axanthism as defined by Bechtel is a hereditary defect of xanthophore pigment metabolism. The result is a decreased amount or absence of red, yellow and the intermediate colors they form. In this defect melanophores and iridophores function normally. The most typical example of an axanthic snake is what is referred to as an anerythristic (the literal translation of this word is "without red"
corn snake. Normal cornsnakes are very colorful including reds, oranges, yellow, brown and black. A corn snake with a xanthophore defect is mostly black and grey. Axanthism, similarly to albinism, can also be the result of a number of different mutations. A mating between two axanthic individuals will not always produce axanthic offspring.
Leucism is commonly confused with albinism with good reason. Both defects will produce a so called white snake. The difference is that while I have shown that not all albinos are white, all leucistic animals are pure white. Leucism is a defect that affects all chromatophores including melanophores and xanthophores. They produce no color whatsoever. The defect is caused by a recessive trait in its homozygous state. This is the only known mutation that causes leucism. So, if you have a white snake, how do you know if it is albino or leucistic? The answer to this is surprisingly easy: an albino snake will have red eyes while a leucistic snake will have darkly colored eyes, probably blue or black. Please use caution when using this to identify a snake! While I have received this information from a book by a well respected herper, I imagine there are always exceptions to the rule.
Piebaldism is the defect I find most fascinating. Piebald means spotted or patched, especially in black and white. The example that stands out for me and probably most of you is a piebald ball python. Unfortunately, little is known about the genetics of piebaldism, except that it is most probably hereditary. Vitiligo is a condition similar to piebaldism. Vitiligo is when a normally colored hatchling loses color as it ages resulting in a snake that looks piebald. The cause of this ontogenetic (acquired during life) condition is unknown. I keep hoping that my ball python will undergo this pigment change (I know the chances are slim, but I can dream, right?)
Melanism is a color variation that results in black snakes that are normally characterized by a color pattern. Melanism is the phenotypic opposite of leucism. Like piebaldism, melanism can occur congenitally or ontogenetically.
The various color anomalies I have discussed are commonly found in the herp trade. We find these snakes fascinating and are willing to pay big prices for them. In our hands these snakes will most likely lead a long healthy life. In nature, on the other hand, these snakes have low chances of survival. Imagine that you are an albino snake, what are the chances you will be able to sneak up on prey unnoticed? What are the chances that a hawk flying overhead will notice you before he notices your normally colored sibling? The fact is that albino and leucistic snakes stick out like a sore thumb in most environments, seriously decreasing their chances for survival. Another factor that can affect snakes with little or no melanin is harmful exposure to ultraviolet radiation. The absence of melanin in these snakes magnifies the detrimental affects of the sun.
I have always considered snakes with color defects interesting. The mechanisms that cause these variations, while somewhat complicated and confusing at times, are interesting too! I have received most of the information from a book by Bernard Bechtel entitled "Reptile and Amphibian Variants." I hope that I have managed to relate some of the information that I have gained about this subject to you.
Bechtel, H. Bernard (1995). Reptile and Amphibian Variants: Colors, Pattners, and Scales. Krieger Publishing Co., Malabar, FL. 206 pp.
