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.

Agency
National Institute of Health (NIH)
Institute
National Institute of General Medical Sciences (NIGMS)
Type
Research Project (R01)
Project #
5R01GM037841-08
Application #
3293653
Study Section
Genetics Study Section (GEN)
Project Start
1986-07-01
Project End
1992-06-30
Budget Start
1990-07-01
Budget End
1991-06-30
Support Year
8
Fiscal Year
1990
Total Cost
Indirect Cost
Name
Duke University
Department
Type
Schools of Arts and Sciences
DUNS #
071723621
City
Durham
State
NC
Country
United States
Zip Code
27705
Uyenoyama, Marcy K; Takebayashi, Naoki (2017) Evolution of the sex ratio and effective number under gynodioecy and androdioecy. Theor Popul Biol 118:27-45
Redelings, Benjamin D; Kumagai, Seiji; Tatarenkov, Andrey et al. (2015) A Bayesian Approach to Inferring Rates of Selfing and Locus-Specific Mutation. Genetics 201:1171-88
Kumagai, Seiji; Uyenoyama, Marcy K (2015) Genealogical histories in structured populations. Theor Popul Biol 102:3-15
Ayres, Daniel L; Darling, Aaron; Zwickl, Derrick J et al. (2012) BEAGLE: an application programming interface and high-performance computing library for statistical phylogenetics. Syst Biol 61:170-3
Fusco, Diana; Uyenoyama, Marcy K (2011) Sex-specific incompatibility generates locus-specific rates of introgression between species. Genetics 189:267-88
Fusco, Diana; Uyenoyama, Marcy K (2011) Effects of polymorphism for locally adapted genes on rates of neutral introgression in structured populations. Theor Popul Biol 80:121-31
Ganapathy, Ganeshkumar; Uyenoyama, Marcy K (2009) Site frequency spectra from genomic SNP surveys. Theor Popul Biol 75:346-54