Presentation Type
Presentation
Faculty Mentor’s Full Name
Brandon Cooper
Faculty Mentor’s Department
Division of Biological Sciences
Abstract / Artist's Statement
Maternally transmitted Wolbachia bacteria infect about half of all insect species. Wolbachia often manipulate host reproduction to increase their transmission. For example, many Wolbachia strains cause cytoplasmic incompatibility (CI) that reduces the viability of embryos fertilized by Wolbachia-infected sperm. Wolbachia infections in females can rescue this incompatibility, providing hosts a relative fitness advantage and facilitating Wolbachia spread to high frequencies. Notably, CI does not always cause complete embryonic death. Many Wolbachia strains, like wMel that infects model Drosophila melanogaster, cause only weak or moderate CI and occur at intermediate frequencies. The contributions of environmental conditions, and Wolbachia and host genomes, to CI strength remain unresolved. Here, I investigate temperature effects on wMel CI strength using both uninfected and infected adult D. melanogaster genotypes sampled from tropical and temperate populations in Australia. I reared male flies at 20oC or 25oC for three generations and females for two generations. These temperatures fall within the range that I observe along the Australian cline. I found that tropical and temperate wMel-infected males cause stronger CI at 20°C, but temperate males cause about 20% stronger CI at 20°C than do tropical males. These data suggest that temperature significantly impacts CI strength, and that wMel-infected genotypes that evolved in relatively cool temperate climates cause particularly strong CI in the cold. To dissect the contributions of host and Wolbachia genomes to this variation, I am now reciprocally introgressing temperate and tropical host and Wolbachia genomes. This strategy will pair tropical Wolbachia with temperate nuclear host genomic backgrounds, and vice versa, to test how Wolbachia and host genomes influence CI strength. I discuss how these results increase our understanding of thermal effects on CI strength, and more broadly, I consider how my findings might explain variation in Wolbachia infection frequencies in global host populations situated in different climates.
Category
Life Sciences
Temperature modulates Wolbachia-induced cytoplasmic incompatibility in Drosophila melanogaster
Maternally transmitted Wolbachia bacteria infect about half of all insect species. Wolbachia often manipulate host reproduction to increase their transmission. For example, many Wolbachia strains cause cytoplasmic incompatibility (CI) that reduces the viability of embryos fertilized by Wolbachia-infected sperm. Wolbachia infections in females can rescue this incompatibility, providing hosts a relative fitness advantage and facilitating Wolbachia spread to high frequencies. Notably, CI does not always cause complete embryonic death. Many Wolbachia strains, like wMel that infects model Drosophila melanogaster, cause only weak or moderate CI and occur at intermediate frequencies. The contributions of environmental conditions, and Wolbachia and host genomes, to CI strength remain unresolved. Here, I investigate temperature effects on wMel CI strength using both uninfected and infected adult D. melanogaster genotypes sampled from tropical and temperate populations in Australia. I reared male flies at 20oC or 25oC for three generations and females for two generations. These temperatures fall within the range that I observe along the Australian cline. I found that tropical and temperate wMel-infected males cause stronger CI at 20°C, but temperate males cause about 20% stronger CI at 20°C than do tropical males. These data suggest that temperature significantly impacts CI strength, and that wMel-infected genotypes that evolved in relatively cool temperate climates cause particularly strong CI in the cold. To dissect the contributions of host and Wolbachia genomes to this variation, I am now reciprocally introgressing temperate and tropical host and Wolbachia genomes. This strategy will pair tropical Wolbachia with temperate nuclear host genomic backgrounds, and vice versa, to test how Wolbachia and host genomes influence CI strength. I discuss how these results increase our understanding of thermal effects on CI strength, and more broadly, I consider how my findings might explain variation in Wolbachia infection frequencies in global host populations situated in different climates.