Gerbil Genetics ~ Section 2

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Gerbil Mutations

If we take a look at the known mutations in the gerbil, at the time of writing this there are nine known mutations that change the coat colour, two responsible for patterning,and two that affect the coat structure.  Since its introduction into captivity in 1935 the majority are inherited recessively, bar three, these are Dominant Spotting, Semi-Dominant Lethal Spotting (patterning genes) and Rexoid.   A successful coat mutation is an exceptionally rare event in many species and occurs when their DNA gets modified in some way. Alterations in cells happen all the time, however these abnormal cells don't usually prosper. DNA repair mends most changes before they can become permanent mutations, and many organisms have specific mechanisms for eliminating these abnormal cells. Sometimes, if this alteration occurs early on in an animal's development, such as in the sperm, ova or zygote, the abnormal cell may succeed and have a chance of survival.

When considering a mutation that affects just the hair colouring in an animal, and not one that can also cause a problem elsewhere in the animal's development, the odds will increase as to whether the chances of this altered gene will survive. In certain instances a mutation that affects the hair or coat colour, may also go on to cause detrimental effects to the normal functioning of the organism. Most mutated genes are also recessive in nature, so the individual with this mutation still has to go on to reproduce successfully. If this has been accomplished, two of the descendents will have to reproduce again before you see the mutation surface once more. Over a relatively long time period these mutated genes will then have to be built up in the population, and that's all providing whether the mutation is actually beneficial for the species.

You can now begin to see how such a rare occurrence a successful mutation really is, and appreciate how high the odds are at a new mutation eventually succeeding!

So what exactly is a mutation?

Now that we've been on a cellular journey into a gerbil's inner ear, we know that every single cell in a gerbil's body contains a nucleus. The nucleus itself contains a number of chromosomes containing DNA. If we look closely along these chromosomes, we see that coded within their DNA are a series of genes. These genes create specific proteins. The proteins that are created by genes have very specific functions, which are very wide ranging. There are many examples of this, and we have seen that sometimes they act as a catalyst to help another process to take place within the body, or they can just as easily be used to create something, such as the protein collagen, which helps make body tissues both strong and flexible, or keratin which is responsible for growing hair and nails, and let's not forget about pigment enzymes which give rise to our gerbil's eye and fur colours. In essence, this means that the genes that lie within the chromosomes are responsible for a whole range of differing processes that take place within an organism's body, and the processes rely on groups of genes to produce specific proteins to enable them to take place, either producing hormones, body tissues or even a body characteristic. In the case of the gerbil, the characteristic we are interested in is their hair, or more specifically, their coat colour and coat structure.

The proteins that are produced by the coding of DNA are very specific in nature, so if the sequence of their DNA is altered, even slightly, this can affect the proteins function by either partially stopping, stopping altogether or even completely altering the protein that is produced. This change in the DNA is referred to as a "mutation".

For an organism to function properly, each individual cell depends on differing proteins to function in the right place and at the right time. If a mutation occurs in a protein that plays a critical role in the body, a medical condition will result, which is known as a genetic disorder. However most mutations have little impact on health, for example, they may only alter a genes DNA base sequence (see the flash movie here to learn about bases) but will not alter the protein function that is made by a gene. In most cases, as mentioned earlier, mutations that could represent a genetic disorder are repaired by the DNA repair system of a cell. Individual cells have several pathways in which enzymes recognise and repair DNA, and because DNA itself is subject to damage and mutation in many ways, the whole process of DNA repair is an important factor in protecting the body from disease.

In hereditary diseases, we are dealing with a mutation that is present in a germ cell, which in turn will give rise to offspring carrying the mutation in all of its cells. However a mutation occurring in a somatic cell of an organism will cause this mutation to be present in all the descendents of this cell, and certain mutations can cause the cell to become malignant, which will then gives rise to cancers.

It has also been shown that mutation rates will vary from species to species, and evolutionary biologists theorise that higher mutation rates are beneficial to a species in certain situations, because they allow the organism to adapt and evolve  quickly to an ever changing environment. We can see this with bacteria that are repeatedly exposed to antibiotics, and the selection of resistant mutants can result in strains of bacteria that have a higher mutation rate than the original population. In science these are referred to as mutator strains.

In all wild populations of animals there will always be some forms of slight variations in their DNA, and animals that are radically different from the norm may not fair so well for obvious reasons. However some mutations or variations in the DNA can have advantages that benefit the species long term. Mutations create variations in the gene pool, and natural selection eradicates the less favourable mutations from the gene pool. The favourable types of mutations accumulate in the gene pool, which over time result in evolutionary change within the species. Imagine a butterfly species that through ultraviolet radiation from the sun, produced a change of wing colour in its offspring. Now in most instances this wouldn't do the species any good, and there was certainly no purpose for it at the molecular level, but if this change of colour made it better for the butterfly to evade predators, and was also effective camouflage for the butterfly, then this mutation increases the survival rate.  Through successful reproduction, this mutation will then be passed on to its offspring. Over time the number of butterflies with this mutation will form a large percentage of the original species population.

Diseases or parasites which take advantage of an animal's specific protein may not fair so well if that protein had been altered due to a mutation, and due to this occurring they maybe resistant to the disease or the parasite. These variations in DNA can benefit the species over time. An extreme example of this in humans would be the recessive mutation that causes sickle cell disease. This disease is common in sub-Saharan Africa, where malaria occurs frequently, however it can still occur in other ethnic populations. As a result of this, those with one allele of the sickle cell disease are resistant to malaria since their red blood cells are not affected by the parasites. Those with two alleles, although resistant to malaria, have the accompanying sickle cell disease which is extremely debilitatating and considerably reduces their lifespan. This mutated allele has incomplete dominance, which means that even individuals who have just one mutated allele will still retain immunity to the disease. Although the positive side effect of this mutation is beneficial, and Mendelian laws makes it possible for some people to carry the advantages without the disadvantages of full blown sickle cell anaemia, there would need to be further mutations to solve the problem of the full blown disease in the population.

A very small percentage of all mutations though do have a very positive effect, and these lead to new versions of proteins that help the organism to adapt and survive in a changing environment. In humans we have an example of this with a specific 32 base pair deletion CCR5 (CCR5-Δ 32) which results in HIV resistance to homozygotes and delays the onset of AIDS in heterozygotes. The CCR5 mutation is relatively common to people of European descent. There exists a theory that maybe a reason for the relatively high frequency of CCR5-Δ 32 in the European population is that it gave resistance to the bubonic plague in mid-14th century Europe. People who had this mutation survived the plague, so the frequency of the mutation increased in the population. This could also explain why this mutation isn't present in African populations, as bubonic plague never reached there. Other theories say that it was selective pressure placed on the mutation by smallpox and not bubonic plague. Either way, it shows how such a specific mutation becomes beneficial to a population over time.

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