This project will explore the hypothesis that the evolutionary function of incompatibility systems is to serve as a eugenic mechanism for the improvement of offspring quality. Under this view, parents preferentially invest in offspring of high quality by inhibiting the conception of gestation of offspring that are inbred at specific antigen loci. Such antigen loci can serve as prospective indicators of offspring quality if they exhibit associations with genetic factors that determine viability or fertility. The proposed work will be directed toward the quantitative analysis of the conditions required for the generation and maintenance of associations between antigens and genetic determinants of offspring quality, and the modification of the expression of incompatibility in response to antigen recognition. Models of the convolution of the major histocompatibility complex (MHC) and the t-complex in the mouse, perhaps the clearest example of the kind of incompatibility system under study, will be investigated through the analytical and numerical study of systems of recursions that explicitly described changes in haplotype frequencies. This exploration will be extended by considering more general forms of viability selection and by permitting recombination between the antigen and viability loci. Once the effect of incompatibility on the generation and maintenance of associates between marker antigens and genetic determinants of offspring quality is understood, the investigation of the evolution of incompatibility itself can begin. The modification of the expression of incompatibility in response to the associations will be addressed. The evolutionary principles developed for the analysis of mammalian incompatibility systems will be applied to the study of the origin of gametophytic and sporophytic self-incompatibility in angiosperms. Under the conceptual framework adopted in this project, modifiers that reduce the age of onset of deleterious effects can serve a eugenic function by permitting the reallocation of parental investment in offspring with better prospects. Models will be devised to explore the evolution of interspecific incompatibility in plants, and the modification of the timing of expression of genetic diseases.
