ABSTRACT
All genetic variation originates from mutations (see Section B5), which are changes in the sequence of bases in the DNA (or RNA of RNA viruses). These usually destroy the allele’s ability to function, and so are usually detrimental to the fitness of the genotype. Null mutations are due to complete destruction of the gene’s function, typically by deletion. Stop codons (nonsense mutations) or frameshifts early in the coding sequence, or point mutations changing essential amino acids (e.g. in enzyme active sites) have similar effects. All loss-of-function alleles can be considered together. They are recessive if a single copy of a functional allele is sufficient to produce a normal phenotype. They are usually deleterious (often lethal) when homozygous, and cause the typical human genetic diseases. Some null
Source of variation
In some circumstances (e.g. a heterogeneous habitat) individuals which are different from each other can exploit the range of habitats and reduce competition. Common phenotypes which exceed their ideal habitat will face more competition than rare phenotypes which have surplus habitat. A range of genotypes will persist. Disease strains adapted to common genotypes will be less harmful to rare genotypes, again making rare genotypes fitter.
