| Summary: | Gentoo Penguins (Pygoscelis papua) are marine mesopredators facing threats from anthropogenic environmental change, habitat loss, fisheries pressure, pollution, direct disturbance at colonies, and introduced pathogens. These philopatric seabirds breed across the largest geographic and latitudinal range of any penguin taxon. Given the large biophysical range of Gentoo Penguin habitats, evolutionary theory posits that localised biotic and abiotic interactions would place differential pressures on distinct populations of the species, affecting their genotypes and phenotypes. The host-pathogen interface is one such biotic interaction known to shape evolutionary trajectories. This thesis employs molecular techniques to examine the role of geographical variation on the genetic diversity of (I) the penguin as a host and (II) its enteric viruses, bacteria, and eukaryotic parasites. In this work, I uncovered strong host phylogeographic and population genetic structure according to neutral, mitochondrial, and immune gene (Toll-like receptor, TLR) markers. I also present experimentally-supported evidence of positive selection on TLR5, which points to localised pathogen-driven adaptation. Given the limited understanding of the pathogens circulating in modern Gentoo Penguin habitats, I also undertook parallel sequencing-based screening surveys to report novel viral, bacterial, protozoan and helminthic sequences associated with these seabirds and their sympatric species. Alongside undescribed diversity, I found evidence of greater-than-expected connectivity among the enteric microbes of spatially separate and genetically disparate Gentoo Penguins, as well as Pygoscelid-wide microbe commonalities. This research demonstrates the importance of studying species complexes and biotic interaction at the large scale, particularly in the face of emerging threats and the challenges inherent to wildlife disease monitoring in these remote habitats.
|
|---|