Search

We have argued that sexual reproduction arose very early in the evolution of life as a way of overcoming informational damage or loss through recombinational repair. As organisms became more complex and genome information content expanded, diploidy, at first transient, became the predominant way of coping with increased vulnerability to mutation. This allowed further genome expansion. Once such expansion had occurred, however, diploidy became essentially irreversible, since reversion to haploidy would lead to expression of accumulated deleterious recessive alleles. This expression of recessive alleles also imposes a stiff penalty on organisms that experiment with close inbreeding forms of recombinational repair. A consequence of sex is that fitness (defined as per capita rate of increase) is density dependent. At low population density, fitness declines due to increased costs of finding a mate. This fundamental constraint on population increase can inhibit evolutionary success of the best adapted species if it is small in numbers. Sexual reproduction also tends to eliminate new coadapted genotypes within a species by breaking up their coadapted gene complexes; this also contributes to the cohesion of species. In general, we think the existence of species and their characteristic cohesion and stability over time are direct consequences of sex; and sex in turn is a consequence of the need to overcome gene damage through recombinational repair while at the same time masking the deleterious effects of mutation.

The two fundamental aspects of sexual reproduction, recombination and outcrossing, appear to be maintained respectively by the advantages of recombinational repair and genetic complementation. Genetic variation is produced as a by-product of recombinational repair, but it may not be the function of sexual reproduction.