부산대학교 도서관

Bacteria have been evolving and adapting in different hosts and environments for millions of years. Most human infections are zoonotic, occurring mainly in animals but also being transmissible to humans. Humans and animals have been living together for thousands of years and been sharing or retaining their own bacterial populations. Bacteria can adapt in new hosts and respond to different selective pressures but not all bacterial species are found in all hosts and environments. The genetic mechanisms that promote these adaptations are not fully understood. The work presented in this thesis investigates the genomic and phenotypic adaptations that promote colonization/proliferation of bacteria of the genus Campylobacter and explores variation at the species, lineage and gene level. Pangenomic comparative analyses revealed core and accessory gene variation highlighting the importance of gene gain and loss in the evolution of this species and the use of genomics in identifying molecular markers to monitor lineage specific in vivo infection experiments. Campylobacter are highly recombinogenic, thus a focus has been given on quantifying recombination in the genome. A detailed analysis of recombination has shown the proportion of the mobile genetic elements (mobilome) in the Campylobacter genus and pinpointed genes associated with host adaptation. Additionally, analysis of Campylobacter resistomes between species, lineages, hosts and environments revealed multidrug resistant (MDR) genomic islands (GIs) and the involvement of plasmids in horizontal gene transfer (HGT). This work has provided evidence of interspecies recombination between different species that share the same hosts and the genes associated with them. The work in this thesis has broadened understanding of how genomic plasticity can allow these versatile bacterial pathogens to adapt into new niches and environments.