Maternally Inherited Endosymbiotic Bacteria Of Drosophila : Spiroplasma and Wolbachia

Maternally inherited endosymbionts are ubiquitous among insects and are known to influence the ecology and evolution of a host species. As such, burgeoning evidence exemplifies their effect on host biology through reproduction, nutrition, resistance to pathogens, and heat tolerance. Many inherited symbionts are not guaranteed passage to a new host generation, and therefore can be lost from a host population. To circumvent loss, certain inherited symbionts have evolved the ability to manipulate host reproduction to enhance their transmission. Two common strategies used to do so are: male-killing, where sons of infected females die during embryogenesis; and cytoplasmic incompatibility (CI), which leads to conditional male sterility that can be reversed by mating with a female of the same infection type. Both phenotypes selectively favor female lineages, as heritable symbionts are only transmitted through them. Many heritable symbionts from the bacterial genera Spiroplasma and Wolbachia infect Drosophila. The model organism D. melanogaster, in particular, is naturally infected by a male-killing Spiroplasma strain and weak CI-inducing Wolbachia strain.

Unlike other bacteria, infections of inherited symbionts remain during the life span of the host. This is energetically costly to the host, and yet these well adapted microbes persist in host populations. Many inherited symbionts provide condition dependent benefits (i.e., resistance to pathogens) to the host, to alleviate the cost of infection. Heritable symbionts typically transmit through the egg cytoplasm, and therefore rely on the female host to replicate and enter an egg. I performed quantitative PCR on Spiroplasma strains with and without the male-killing phenotype, to trace bacterial replication in reproductive females. My results suggest, in contrast to previous studies, that there is no evidence for the correlation between the male-killing phenotype and densities. I also compared maternal mRNA found in eggs of Spiroplasma and Wolbachia infected females to determine whether these symbionts alter gene expression of the female during oogenesis. I used RNA-sequencing and bioinformatics tools to determine differential maternal gene expression due to infection. The results suggest that Spiroplasma causes expression changes in genes, that code for a protein incorporated into the vitelline membrane of the oocyte, involved in pre-mRNA splicing, and a candidate gene for the mechanism of male-killing, involved in the sex determination pathway of Drosophila. Wolbachia infection had a minimal effect on maternal gene expression.