‘A mutation is a change in the DNA at a particular locus in an organism.’ Mutation plays an important role in evolution and is the ultimate source of all genetic variation. It is salient as the introductory step of evolution because it creates a new DNA sequence for a particular gene, creating a new allele. Gene mutations occur very rarely but its rate can be artificially increased by mutagenic agents such as mustard gas, x-rays and ultraviolet light to give induced mutations.
Genetic mutations can be classified in two major ways: hereditary and somatic. Hereditary mutations are present virtually in every cell in the body and are inherited from a parent. Due to their presence in the parent’s gametes, the mutations are also referred to as germline mutations. If a mutant gene is passed onto offspring, when growth occurs due to mitosis, the mutation will be present in all cells. The other type of mutations is somatic (acquired). These occur during a person’s life and are therefore present only in some cells. These can be caused by environmental factors such as ultraviolet radiation from the sun, or due to an error made during cell division, which is called non-disjunction. Somatic mutations cannot be passed to offspring due to the mutations not being present in gametes.
A number of regions of DNA possess dominance determining when and where genes are turned ‘on.’ Occurring mutations in these parts of the genome can substantially change the way the organism is built; a mutation in a control gene can cause a cascade of effects in the behaviour of genes under its control. An example of a control gene is hox genes. They are found in a number of animals like humans and designate where the head goes and which regions of the body grow appendages. Such genes assist in the directing of the body’s unit construction eg. segments, limbs, and eyes. Thus evolving an extensive change in basic body layout may not be so unlikely; it may simply require a change in a Hox gene and the favour of natural selection.
‘Mutations can be either beneficial, neutral, or harmful for the organism.’ Though it is said that factors in the environment an influence on the rate of mutation, they are not thought to influence the direction of mutation. This means that exposure to harmful chemicals may increase the mutation rate, but will not cause more mutations that make the organism resistant to those chemicals. In this respect, whether a certain mutation occurs or not is unallied to how serviceable that mutation would be, proving the concept that mutations are random. For example, in the U.S. where people have access to shampoos with chemicals that kill lice, a lot of lice that are resistant to those chemicals are commonly encountered. Two possible explanations can arise for this:
‘HYPOTHESIS A - Resistant strains of lice were always there — and are just more frequent now because all the non-resistant lice died.
HYPOTHESIS B - Exposure to lice shampoo actually caused mutations for resistance to the shampoo.
In 1952, Esther and Joshua Lederberg performed an experiment that aided in showing that mutations are random. They focused on the idea that bacteria grow into isolated colonies on plates. These colonies have the ability to reproduce from an original plate to a new plate by the process of ‘stamping’ (stamping the original plate with a cloth and then stamping empty plates with the same cloth). Bacteria from each colony are picked up on the cloth and then deposited on new plates. This led to Esther and Joshua hypothesising that antibiotic resistant strains of bacteria surviving an application of antibiotics had the resistance before their exposure to the antibiotics, not as a result of the exposure. Their experimental set up is summarised below:
This shows that before the encounter of penicillin the resistant bacteria were present in the population thus did not evolve resistance in response to the exposure of the antibiotic. Moreover, from the evidence available, we can hence deduce that mutations might therefore preferentially form around existing ones.
By Gaya Giritharan, 10F