|Institution:||University of New South Wales|
|Department:||Biotechnology & Biomolecular Sciences|
|Keywords:||Maternal inheritance; Wolbachia; Mitochondria|
|Full text PDF:||http://handle.unsw.edu.au/1959.4/53783|
Similarly to other cytoplasmic genetic elements, intracellular endosymbionts of animals are passed to the next generation of hosts through the egg. This mode of transmission is key to understanding the evolution of these symbiotic associations. For instance, maternal inheritance creates a sexual asymmetry, as genetic variants that are advantageous to females would persist even when harmful to males. Wolbachia are well known for using such sexual asymmetry to their advantage: by actively reducing the reproductive chances of non-infective hosts, they often increase the relative fitness of infected matrilines. However, so long as these genetic elements prevent the normal transmission of host genetic material to the next generation, there would be antagonistic selective pressure over the reproductive phenotype from the host. This means that Wolbachia-related parasitic phenotypes, similarly to sex-antagonist mitochondrial mutations, would be likely attenuated by compensatory adaptation. Despite being often perceived as parasites, emerging evidence on beneficial effects of Wolbachia offers new perspectives on the nature of Wolbachia-host interactions. Similarly to the current understanding on the maintenance of functional mitochondrial genetic variation, Wolbachia that pose advantages contingent to the host nuclear background and the environment may be selectively favoured and maintained at equilibrium, even in the face of attenuation of reproductive manipulation phenotypes. This thesis explores various aspects of the interaction between cytoplasmic (namely Wolbachia and mitochondria) and nuclear genomes using Drosophila flies as models. Additionally to their well-characterised mitochondrial genomes, Drosophila can serve as host to a variety of Wolbachia infections with markedly distinct phenotypes, which provides the opportunity to test hypothesis regarding host adaptation to phenotypic effects of cytoplasmic variants. Three major conclusions can be drawn from this thesis: Firstly, phenotypes related to cytoplasmic genetic variants can be highly contingent on the sex, physiological state and nuclear background of the host, as well as the environment. Secondly, adaptation of the host genome to cytoplasmic genetic variants is linked to their effects on the organismal fitness. Finally, beneficial effects of cytoplasmic variants that are contingent on the host genetic background and the environment may explain their polymorphism in natural populations.