Postdoctoral Researcher University of Kentucky Tucson, Arizona
Insects harbor intracellular, maternally-transmitted bacterial symbionts that may manipulate host reproduction to favor infected females. A common form of reproductive sabotage is cytoplasmic incompatibility (CI), in which the symbiont modifies infected males, sabotaging reproduction such that crosses with uninfected females produce inviable offspring. While the CI symbiont Wolbachia has been relatively well characterized, relatively little is known about an independently-evolved CI-inducing symbiont lineage, Cardiniumhertigii. Cardinium is a common CI-inducing symbiont, infecting ~10% of arthropods, including minute parasitoid wasps in the genus Encarsia. Using antibiotic treatments, I found that the Cardinium strain cEper1 modifies its host, Encarsia suzannae, during pupation. I used fluorescent in-situ hybridization (FISH) to reveal cEper1 localization within developing E. suzannae testes during the CI modification window. Cardinium cells are abundant in testes and infect most sperm cells but are removed from these cells during the sperm maturation process, which is completed prior to adulthood. These results indicate that Cardinium modifies Encarsia sperm cells during their maturation process in the pupal stage. Next, I explored the CI timing and cellular localization of a second CI-inducing strain of Cardinium in E. partenopea. This second strain, cEina3, is present at a low-density within its host and also modifies its host during pupation but does not infect sperm cells. Instead it infects somatic cells in the seminal vesicle, a sperm storage organ. Finally, I highlight future work identifying Cardinium CI factors using LC-MS/MS.
