Exploring the Impact of Bottleneck History and Pathogen-mediated Balancing Selection on MHC Class II DRB Nucleotide Variability in Bottlenecked and Unbottlenecked Marine and Terrestrial Mammals
Files
Date
Authors
Journal Title
Journal ISSN
Volume Title
Publisher
Access Restrictions
Abstract
Genetic variability at the major histocompatibility complex (MHC) is thought to play a fundamental role in controlling the array of parasites a host can recognize and fight against. Previous research endeavors, which have explored separately the impact of population bottlenecks and pathogen-mediated balancing selection on MHC variability, have failed to account for the effect that a combination of these factors has on MHC variability. This thesis utilizes meta-analyses of bottlenecked and unbottlenecked mammals from both marine and terrestrial environments to elucidate the roles that bottleneck history and pathogen-mediated balancing selection play simultaneously in maintaining MHC diversity. Generally, a population bottleneck causes a decrease in genetic variability at neutral markers; however, there is currently evidence to support both the maintenance and decrease of MHC polymorphism following a population bottleneck. Similarly, a general consensus has not been reached regarding the effect of environment type on MHC variability; however, it is believed that terrestrial environments are home to a greater number of parasites which lead to an increase in MHC diversity. The linear models developed in this thesis indicate that there is significant interaction between bottleneck history and environment type when considering how these factors influence nucleotide diversity, but only when selection pressure from parasites is accounted for. These results confirm that it is of particular importance to restrict commercial hunting/fishing of marine mammals in order to prevent an anthropogenically-induced bottleneck event that could potentially decrease the probability of survival of marine mammal populations through a decrease in genetic variability at immune genes.