Genetics
Learn basic genetics for reptilekeepers and breeders
By Vincent J. Lynch
It seems nearly every reptile species commonly kept and bred by hobbyistss these days has at least one genetic color or pattern morph. With some species, such as ball pythons, corn snakes and leopard gecko, the number of morphs is truly overwhelming. This popularity has increased the use of genetic terms, which describe how morphs are inherited and predict the outcomes of morph crosses. Unfortunately, the morph explosion also has introduced confusing and sometimes mysterious genetic jargon and math into the hobby. But the genetics of reptile color and pattern mutations don't have to be difficult. Some biology basics make them easy to understand.
Building a Foundation
Animals consist of hundreds of millions of cells. Within each cell is a special compartment called the nucleus, and it houses the cell's genes. The sum of those genes - and all DNA between them - is called the genome. Except for sperm and eggs, each animal cell has two complete copies of the genome. One is inherited from the mother, and the other comes from the father. In principle, each copy of the genome;s estimated 60,000 genes is exactly the same. In reality, however, some copies have small differences between them. These are called mutations.
Mutations arise during the production of reproductive cells. The genome is copied and packaged into sperm and eggs. This process is nearly perfect, but mistakes happen. Consider the photocopy of a picture. Imagine copying the photocopy and then copying that copy. Do this long enough, and you'll notice small imperfections slowly distort the original image. Luckily, evolution has devised an error-checking system. Like a good proofreader, it compares a newly copied genome to the original and corrects mistakes. Yet even this mechanism isn't perfect. Mistakes can happen in nearly 3 billion places, so a few errors will slip through. Each new sperm and egg contains a handful of mutations.
Most mutations occur in functionally unimportant regions of the genome. They make no contribution to the animal's health or appearance. However, gene mutations disrupt a gene's normal function. If the mutation occurs in a gene important for pigment production, pigment storage or pattern formation, a new morph is created.
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For example, albinism results from a mutation that inactivates a gene called tyrosinase, which is vital to black pigment formation. But not all mutations are deleterious. Some can actually benefit the organism. Consider antibiotic-resistant bacteria. Their resistance stems form a mutation that enables an enzyme to break down antibiotics. Bacteria with the mutation have a powerful advantage when exposed to antibiotics. They survive and reproduce - even if that is bad for us humans.
Fortunately, a single gene mutation rarely causes things to go horribly wrong. Remember, each gene has two copies. If one copy goes mutant ,the backup compensates and takes over. These are two forms of the gene, one normal and one mutant, and these alternative forms are called alleles. Some alleles are dominant to others, which means they can completely cancel the effects of another allele.
Consider the albino example again. In this case there are two alleles. The normal allele is dominant to the mutant allele. This means neither an animal with two normal alleles, nor an animal with one normal and on mutant copy exhibits the albino trait. Both animals look completely normal. Only an animal with two mutant alleles will be an albino.
Suppose a gene has only two alleles like our albino. This pair can be combined in four possible ways. Let's call the normal allele of the albino gene "A" and the mutant allele "a". Alleles can be combined as AA, Aa, aA and aa. These allele combinations are called genotypes. Both Aa and aA are essentially the same, so we can reduce the complexity a little and say there are three genotypes: AA, Aa and aa. homozygous animals have the same alleles, such as AA and aa. Heterozygous animals have mixed alleles, such as Aa.
Remember, the normal allele (A) is dominant to the mutant allele (a) in our albino example, so the three genotypes can have one of two appearances. These appearances are called phenotypes. Because the normal allele (A) can completely cancel the mutant allele (a), animals with AA or Aa look the same. Without a functioning copy of the gene, animals with aa will be albinos.
Crossing Animals
Being able to predict the outcome after crossing two morphs is valuable tool to have. Although this power is fundamental to modern biology, it was not possible before the late 19th century. The major breakthrough came from the careful work of Austrian monk and naturalist Gregor Mendel. Named the "father of genetics". Mendel cultivated pea plants with several variable traits, including flower color, seed color and seed shape. Keeping careful records of parent and offspring appearance from more than 28,00 crosses, and he was able to make generalization on inheritance and predict the outcome of crosses.
Mende;s work went virtually unnoticed for half a century. It was not until 1900 that Reginald Punnet "rediscovered" Mendel's contributions and put them to use. Although Punnet made many contributions to the field of genetics, he is know for developing the Punnet square, a tool used for predicting offspring's genotypes and phenotype when the genotype of the parents is known.
Using the albino animal example again, let's cross it with a normal animal. The albino parent's genotype can only be aa. Assume the genotype of the normal parent is AA. This means an albino can only make sperm or eggs with the genotype a, and the normal animal can only make reproductive cells with A genotype. if you breed the animals, the offspring inherit an a allele and A allele respectively. Carrying the genotype Aa, all offspring are heterozygous for albino.
This outcome is easy to predict, but outcomes become more complicated when two heterozygous animals, or "hets", are crossed. This is where the Punnet square becomes handy. Breeders can useit to determine the genotypes and phenotypes of offspring as well as predict the probability of producing them.
Breeding hets of our albino example yield three possible outcomes: AA, Aa and aa. This example is relatively simple, but crosses can be much more complicated. Consider producing a designer morph such as a snow. These animals are albino and anerythristic, which literally means without erythrin, a red pigment. "Anery" animals lack red color and are usually various shades of black, white and gray.
The initial cross produces normal-looking animals that carry an allele for both albino (a) and anery (r). In other words, their genotype is AaRr, and they are double heterozygotes.
Constructing a Punnet square for double het is similar to a single het (our albino example) except now we have four possible genotypes for sperm and eggs: AR, aR, Ar and ar. Instead of four cells and four possible outcomes for our Punnet square, we have 16 cells and 16 possible outcomes. Only one of the 16 is the snow.
Things get considerably more complicated when three genes are involved. Crossing a triple het has 64 possible genotypes, and only one exhibits the trait you're after. You probably get the picture.
More Complicated Crossings
In our albino example, the alleles were clearly dominant or recessive, but this is not always the case. Simple genetic traits (such as albinos and anerythristics) can be explained by dominant and recessive alleles. Complex traits cannot be explained so easily. Several kinds of complex traits exit, but only a few are important for reptile breeding, such as incomplete dominant, co-dominant and multi-genetic traits.
Sometimes the appearance of the heterozygote (Aa) is different from both homozygotes (AA and aa) and lies somewhere in between the appearance of the two homozygotes. In this case, neither allele is able to cancel the effects of the other, so their effects blend. This type of inheritance is called incomplete dominance. It occurs because a mutation change how one of these genes functions but does not completely destroy it. Each allele in the hetrozygot will contribute something to the phenotype.
A good example of incompletely dominant traits has shown up in corn snakes. These snakes have three alleles of the tyrosinase gene: A, a and u. The genes are responsible for making black pigment. AA individuals are normal, aa are albino, and uu are ultra hypo, which is a very extreme - nearly albino - form of hypomelanism.
The incompletely dominant trait appears when an albino (aa) is bred to an ultra hypo (uu). Because the alleles cannot cancel each other out, the offspring have a third phenotype that splits the difference between albino and ultra hypo. These "au" individuals have been called "ultra amel" or "ultramel" and have more dark pigment than an albino, but much less black pigment than a normal animal. Thus the alleles a and u are incompletely dominant to each other, yet both are recessive to A.
Unlike incompletely dominant traits, trait co-dominance is the special situation when both alleles are expressed at the same time, so the phenotype is a mixture - not a blending - of both homozygous phenotypes. In this case, both alleles are functional, but they ahve mutations that lead to difference in where they are expressed (or turned on). There are few examples of true co-cominant traits in reptiles, but classic examples include human blood type and roan coat color in horses and cattle.