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The adaptive function of sex remains, today, one of the major unsolved problems in biology. Fundamental to achieving a resolution of this problem is gaining an understanding of the function of meiosis. The sexual cycle in eukaryotes has two key stages, meiosis and syngamy. In meiosis, typically a diploid cell gives rise to haploid cells. In syngamy (fertilization), typically two haploid gametes from different individuals fuse to generate a new diploid individual. A unique feature of meiosis, compared to mitosis, is recombination between non-sister homologous chromosomes. Usually these homologous chromosomes are derived from different individuals. In mitosis, recombination can occur, but it is ordinarily between sister homologs, the two products of a round of chromosome replication. Birdsell & Wills (2003) have reviewed the various hypotheses for the origin and maintenance of sex and meiotic recombination, including the hypothesis that sex is an adaptation for the repair of DNA damage and the masking of deleterious recessive alleles. Recently, we presented evidence that among microbial pathogens, sexual processes promote repair of DNA damage, especially when challenged by the oxidative defenses of their biologic hosts (Michod et al., 2008). Here, we present evidence that meiosis is primarily an evolutionary adaptation for DNA repair. Since our previous review of this topic (Bernstein et al., 1988), there has been a considerable increase in relevant information at the molecular level on the DNA repair functions of meiotic recombination, and this new information is emphasized in the present chapter.

Meiosis as an Evolutionary Adaptation for DNA Repair