| Description |
Major histocompatibility complex (MHC) molecules playa central role in immune recognition by presenting small peptides (antigens) to the T-Iymphocytes. The genes that encode the MHC molecules are the most polymorphic loci known for vertebrates. The exact evolutionary mechanism responsible for this diversity remains unknown. Many theories explaining how MHC diversity can be maintained have been developed but empirical data supporting these theories are lacking. One reason for the absence of data is that studies are typically done under benign, laboratory conditions. These conditions may not include factors that maintain MHC diversity. Many of the theories about MHC diversity postulate that the effects of MHC genotype will be most pronounced under pathogen loads and intense intraspecific competition found in natural populations. Consequently, studies in natural populations could provide critical insights into mechanisms responsible for MHC diversity. However, this requires a fast and simple genotyping system for MHC in wild populations. Recently, a microsatellite-based genotyping system was reported for inbred strains of mice. The system utilized several MHC-linked microsatellites to give multiple genotype assignments across the complex. The microsatellites offer a rapid, inexpensive way of typing MHC in inbred mice. In this project, the ability of these MHC-linked microsatellites to be used for MHC genotyping of wild mice was tested. I evaluated 32 microsatellite loci for their mendel ian inheritance and scoring reliability. The best 3 were then tested for their ability to genotype wild mice for their MHC. Problems with both scoring reliability and mendelian inheritance led to the conclusion that the MHC-linked microsatellites, as evaluated in this project, cannot genotype wild mice accurately. |
