The adaptive significance of sexuality.
The theory predicts that inbred strains of mice are susceptible to tumor viruses that have escaped immune recognition. The theory implies routine evolutionary extinction of asexual species and that existing parthenogenetic species would have to have evolved recently from sexually reproducing precursors. This could be tested by determining the amount of DNA divergence between parthenogenetic and related sexually reproducing species. In mammals and birds genetic substitutions occur at comparable rates, but the AIDS virus evolves about 10 million times more rapidly. This confirms the basic imbalance of rates of evolution between microparasites and metazoan hosts, which is fundamental to the theory. The organization of most eukaryotic genes into exons and introns facilitates the generation of variety of gene products, and the molecular mechanism is similar to the mechanism that generates antibody diversity in the immune response and antigenic variation in trypanosomes. It has been proposed that noncoding 'selfish' DNA is the ultimate sexually transmitted disease. If this were the case, then asexually reproducing species would have an added advantage. An alternative hypothesis is proposed: noncoding DNA could provide insertion sites for retroviruses that would prevent them from being transcribed and replicated and thus moderate their proliferation much as absorber rods moderate proliferation of neutrons in a nuclear reactor. Flowering plants have pollen selection mechanisms that enforce heterozygosity at one or more loci. It has been proposed that analogous sperm selection mechanisms exist in mammals. Such a process would account for observation of a mysterious excess molecular divergence between different strains of inbred mice.
D000222:Adaptation, Physiological; D000818:Animals; D005075:Biological Evolution; D005260:Female; D006790:Host-Parasite Interactions; D007107:Immune System / Q000502:physiology; D008285:Major Histocompatibility Complex; D008297:Male; D051379:Mice; D008957:Models, Genetic; D011110:Polymorphism, Genetic; D012723:Sex