Consequences of population structure on genes under balancing selection.
This paper describes a new approach to modeling population structure for genes under strong balancing selection of the type seen in plant self-incompatibility systems and the major histocompatibility complex (MHC) system of vertebrates. Simple analytic solutions for the number of alleles maintained at equilibrium and the expected proportion of alleles shared between demes at various levels are derived and checked against simulation results. The theory accurately captures the dynamics of allele number in a subdivided population and identifies important values of m (migration rate) at which allele number and distribution change qualitatively. Starting from a panmictic population, as migration among demes decreases a qualitative change in dynamics is seen at approximately m(crit) approximately equal to the square root of(s/4piNT) where NT is the total population size and s is a measure of the strength of selection. At this point, demes can no longer maintain their panmictic allele number, due to increasing isolation from the total population. Another qualitative change occurs at a migration rate on the same order of magnitude as the mutation rate, mu. At this point, the demes are highly differentiated for allele complement, and the total number of alleles in the population is increased. Because in general u << m<(crit) at intermediate migration rates slightly fewer alleles may be maintained in the total population than are maintained at panmixia. Within this range, total allele number may not be the best indicator of whether a population is effectively panmictic, and some caution should be used when interpreting samples from such populations. The theory presented here can help to analyze data from genes under balancing selection in subdivided populations.
Muirhead
C A
CA
Department of Integrative Biology, University of California, Berkeley 94720-3140, USA. muirhead@socrates.berkeley.edu
D000483:Alleles; D000818:Animals; D005075:Biological Evolution; D003198:Computer Simulation; D005828:Genetics, Population; D006680:HLA Antigens / Q000235:genetics; D006801:Humans; D008285:Major Histocompatibility Complex / Q000235:genetics; D008433:Mathematics; D008957:Models, Genetic; D018521:Plant Physiological Phenomena; D012474:Salmon / Q000235:genetics; D012641:Selection, Genetic
D006680:HLA Antigens