Sexual Selection and Bacteria

The role of symbiotic bacteria in determining their host’s phenotype has become increasingly apparent in recent times. These bacterial communities can influence a range of host traits and fitness correlates. Symbiotic bacteria can alter their host’s immune function, metabolism, reproductive fitness, sexual and social signals as well as behaviour. The amount of research into the host fitness effects of symbiotic bacterial is rapidly increasing, however; few studies are investigating how these effects vary across different host genotypes. This thesis investigates the relationship between host genetic background and bacterial symbionts across a range of sexually selected fitness measures in Drosophila simulans. We focused on two main types of bacterial symbionts; exosymbionts, that consisted of gut bacterial communities and surface bacteria that inhabit the fly cuticle, along with the bacterial endosymbiont Wolbachia pipentis. Wolbachiais known to influence host fitness in a range of ways that vary from parasitic to mutualistic. The nature of these effects has previously been found to depend on both the host and the strain of Wolbachia.Previous work has attributed fitness effects found when curing Wolbachia infection with antibiotics to the change in the Wolbachia infection status. Antibiotic treatment is likely to change other bacterial components of the microbiota alongside removing Wolbachia infection. In chapter 2 I found that antibiotic-caused male sexual-fitness rank changes across genotypes were caused by Wolbachia curing and not altering exosymbiotic bacterialcommunities. In Chapter 3 I found that the level of bidirectional cytoplasmic incompatibility suffered when mating with a standardised tester mate, was dependant on the genotype of the focal host. This effect was true for both focal males and females. In Chapter 4 I tested whether D. simulans populations evolving under elevated or relaxed natural and sexual selection for 38 generations differed in their gut bacterial communities. We found evolving under elevated sexual selection resulted in more diverse gut bacteria for males but not females. We also found sexual selection altered the gut bacterial community composition of both males and females. We found no effects of natural selection on gut microbial communities and no interaction between natural and sexual selection intensity on these communities. In Chapter 5 I found that altering exosymbiotic bacterial communities had fitness effects on both 3males and females. In females these effects were only present when the bacterial communities were altered,not if the bacteria were simply removed. In Chapter 6I found that Wolbachia infection affects female choosiness dependent on the females’genotype. Removing the exosymbiotic bacteria from females had no effect on their choosiness and genotype did not interact with this bacterial treatment. I also found that removing the symbiotic bacteria of females reduces their adult body size,however hosts infected withWolbachia did not experience the same body size reduction with exosymbiont removal. Symbiotic bacteria are playing an important role in many sexually selected fitness traits. The direction and scale of these fitness effects depend on the host’s genetic background. Sexual selection is also able to act on a host’s gut bacteria. This means that a host’s symbiotic bacteria are likely to play an important role in the evolutionary outcomes ofsexual selection. This thesis increases our understanding of the role symbiotic bacteria playinsexual selection.Natural Environment Research Council (NERC

Oligodendrocyte Fate after Spinal Cord Injury

Oligodendrocytes (OLs) are particularly susceptible to the toxicity of the acute lesion environment after spinal cord injury (SCI). They undergo both necrosis and apoptosis acutely, with apoptosis continuing at chronic time points. Loss of OLs causes demyelination and impairs axon function and survival. In parallel, a rapid and protracted OL progenitor cell proliferative response occurs, especially at the lesion borders. Proliferating and migrating OL progenitor cells differentiate into myelinating OLs, which remyelinate demyelinated axons starting at 2 weeks post-injury. The progression of OL lineage cells into mature OLs in the adult after injury recapitulates development to some degree, owing to the plethora of factors within the injury milieu. Although robust, this endogenous oligogenic response is insufficient against OL loss and demyelination. First, in this review we analyze the major spatial–temporal mechanisms of OL loss, replacement, and myelination, with the purpose of highlighting potential areas of intervention after SCI. We then discuss studies on OL protection and replacement. Growth factors have been used both to boost the endogenous progenitor response, and in conjunction with progenitor transplantation to facilitate survival and OL fate. Considerable progress has been made with embryonic stem cell-derived cells and adult neural progenitor cells. For therapies targeting oligogenesis to be successful, endogenous responses and the effects of the acute and chronic lesion environment on OL lineage cells must be understood in detail, and in relation, the optimal therapeutic window for such strategies must also be determined