Viral genomes contain either DNA or RNA. Mutations result from errors during DNA or viral replication, mitosis, or meiosis or other types of damage to DNA (such as pyrimidine dimer caused by exposure to ultraviolet radiation), which then may undergo error-prone repair end joining, cause an error during other forms of repair, or to cause an error during replication (translation synthesis). Mutations may also result from insertion or deletion of segments of DNA due to mobile genetic elements.
Mutations may or may not produce detectable changes in the observable characteristics (phenotype) of an organism. Mutations play a part in both normal and abnormal biological processes including: evolution, cancer, and the development of the immune system, including junctional diversity. Mutation is the ultimate source of all genetic variation, providing the raw material on which evolutionary forces such as natural selection can act.
Mutation can result in different types of change in sequences. Mutations in genes can have no effect, alter the product of a gene, or prevent the gene from functioning properly or completely.
Mutations can also occur in monogenic regions. A 2007 study on genetic variations between different species of Drosophila suggested that, if a mutation changes a protein produced by a gene, the result is likely to be harmful, with an estimated 70% of amino acid polymorphisms that have damaging effects, and the remainder being either neutral or marginally beneficial.
Due to the damaging effects that mutations can have on genes, organisms have mechanisms such as DNA repair to prevent or correct mutations by reverting the mutated sequence back to its original state.[5]
Four classes of mutations are (1) spontaneous mutations (molecular decay), (2) mutations due to error-prone replication bypass of naturally occurring DNA damage (also called error-prone translation synthesis), (3) errors introduced during DNA repair, and (4) induced mutations caused by mutagens. Scientists may also deliberately introduce mutant sequences through DNA manipulation for the sake of scientific experimentation.
One 2017 study claimed that 66% of cancer-causing mutations are random, 29% are due to the environment (the studied population spanned 69 countries), and 5% are inherited.[29]
Humans on average pass 60 new mutations to their children, but fathers pass more mutations depending on their age, with every year adding two new mutations to a child.
Spontaneous mutations occur with non-zero probability, even given a healthy, uncontaminated cell. Naturally occurring oxidative DNA damage is estimated to occur 10,000 times per cell per day in humans and 100,000 times per cell per day in rats.[31] Spontaneous mutations can be characterized by the specific change:[32]
Tautomerize – A base is changed by the repositioning of a hydrogen atom, altering the hydrogen bonding pattern of that base, resulting in incorrect base pairing during replication.[33]
Purine removal– Loss of a purine base (A or G).
Deamination – Hydrolysis changes a normal base to an atypical base containing a keto group in place of the original amine group.
It can be corrected by DNA repair mechanisms; and 5MeC (5-methylcytosine) → T, which is less likely to be detected as a mutation because thymine is a normal DNA base.
Slipped strand non pairing
Denaturation of the new strand from the template during replication, followed by denaturation in a different spot ("slipping"). This can lead to insertions or deletions.
Replication slippage
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