Sex and polymorphism as strategies in host-pathogen interactions.

Abstract Sexual reproduction in a polymorphic population generates ever novel recombinations. It is shown that this variety is essential in preventing pathogens from adaptively breaking through immunological host resistance. The theory explains the extensive polymorphism of wild-type populations and catastrophic diseases in genetically homogeneous cultivars. It offers a new model of the selective forces that maintain sex. It interprets self-incompatibility in angiosperms as a mechanism that maintains polymorphism. An analogous mechanism involving sperm selection based on histocompatibility haplotype is postulated for mammalian fertilization. Mate selection involving odor clues is conjectured for eusocial insects. Population regulation of asexual species through pathogens also involves polymorphism. The proposed theory of polymorphism overcomes difficulties present in the balanced and neutral selection theory of mathematical genetics.

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