Files
Abstract
Insect-microbe symbioses are common in nature. Generally, these symbioses can be categorized into two groups: obligate (primary) symbioses and facultative (secondary) symbioses. The pea aphid, Acyrthosiphon pisum, has become a model system for studying bacterial symbionts because it hosts not only a primary nutritional symbiont, Buchnera aphidicola, but it can also play host to any number of 8 other facultative symbionts. One such symbiont, Hamiltonella defensa, provides its aphid host with protection against the parasitoid wasp Aphidius ervi. Field studies have also found that there is variation in the level of protection that H. defensa provides. This variation has been attributed to differential infection by a bacteriophage named APSE. Different haplotypes of APSE are responsible for different levels of protection while uninfected H. defensa provide no resistance to their aphid hosts. APSE haplotypes vary little from one another in gene content outside of a variable region that contains putative eukaryotic toxin genes. This has led to the hypothesis that protection is due to expression of these phage borne toxin genes that kills the developing wasp larvae in the aphid hemocoel. However, there has been little experimental evidence directly linking toxin genes from APSE to A. ervi death. Furthermore, there has been little work describing how APSE persists within H. defensa and the impact infection has outside of killing A. ervi within the aphid host. This is largely due to the intractability of bacterial symbionts and the complexity of this tripartite symbiosis. Therefore, my work has been to address these gaps in our knowledge through the creation of an in vitro system and functional