Abstract
AbstractPhenotypic plasticity is prevalent in nature and can facilitate the acclimation of organisms to changing environments. Recombination rate is plastic in a diversity of organisms and under a variety of stressful conditions. However, the recent finding that Wolbachia pipientis induces plastic recombination in Drosophila melanogaster was surprising because Wolbachia is not strictly considered a stressor to this host. We investigate the molecular mechanisms of Wolbachia-associated plastic recombination by comparing the ovarian transcriptomes of D. melanogaster infected and uninfected with Wolbachia. Our data suggest that infection explains a small amount of transcriptional variation but specifically affects genes related to cell cycle, translation, and metabolism. We also find enrichment of cell division and recombination processes among genes with infection-associated differential expression. Broadly, the transcriptomic changes identified in this study provide insight for the mechanisms of microbe-mediated plastic recombination, an important but poorly understood facet of host-microbe dynamics.Significance StatementThough it is documented that Wolbachia is associated with increased recombination in D. melanogaster, the underlying mechanisms remain unknown. Here we use ovarian transcriptomics in Wolbachia-infected and uninfected flies to identify candidate genes underlying Wolbachia-associated plastic recombination. We find that infection alters ovarian gene expression in subtle ways, and also identify exciting candidate genes for functional analysis in subsequent work. These candidate genes may be the first step in determining the molecular mechanisms underlying Wolbachia-associated plastic recombination. Moreover, our data contribute to the growing body of knowledge surrounding how Wolbachia affects host gene expression, and highlights how context-dependent these effects are.
Publisher
Cold Spring Harbor Laboratory