View Program - 63rd Annual Drosophila Research Conference

Organisms can defend against pathogens by significantly increasing the diversity of their progeny, so that some progeny are more likely to survive infection. This leads to the prediction that infection should cause an increase in recombination rates. This prediction was confirmed in a published study where female Drosophila melanogaster that were infected with the gram-negative bacteria Providencia rettgeri had increased recombination rates compared to control flies. However, the mechanism of this rate modulation is unknown. Our lab conducted an RNAi screen to identify genes that cause defects during chromosome congression, which identified mustard (mtd) as causing ~40% congression failure. We show this is caused by a 95% reduction in recombination rates, which overwhelms the distributive segregation pathway similarly to mutants that block recombination like c(3)G or meiW68. The mtd gene had previously been shown to be part of the Immune Deficiency (IMD) pathway, which primarily defends against gram-negative bacteria. In that study, they showed that a gain-of-function allele increased the survival rate of flies that were infected with the gram-negative bacteria Vibrio cholerae. These results suggest that the IMD pathway may be what modulates recombination rates in response to bacterial infection. We are testing this hypothesis by measuring if the recombination rate changes caused by P. rettgeri infection depends on mtd function.

Characterization of the Immune Deficiency Pathway during female meiosis in Drosophila melanogaster