Does varying investment in egg production modify immune defense in mated female Drosophila melanogaster?
Authors: Kathleen Gordon 1; Mariana Wolfner 2; Brian Lazzaro 1,3
Affiliations: 1) Department of Entomology, Cornell University, Ithaca, NY; 2) Department of Molecular Biology and Genetics, Cornell University, Ithaca, NY; 3) Cornell Institute of Host-Microbe Interactions and Disease, Cornell University, Ithaca, NY
Keywords: j. fat body; b. oogenesis
In D. melanogaster and many other species, female reproductive investment comes at a cost to immunity and resistance to infection. In previous work, we have shown that D. melanogaster females become more susceptible to bacterial infection within hours of mating and for at least ten days. During mating, the male transfers seminal fluid proteins that change many aspects of female physiology and behavior, including inducing a rapid and sustained increase in egg production. One of these seminal proteins, Sex Peptide (SP), is involved in reducing female immune capacity. At least some of this effect may be due to stimulation of egg production by SP, as female flies without a germline, and who therefore produce no eggs, retain high immune capacity upon mating. Production of yolk protein to provision eggs is one of the major demands of reproduction, and we hypothesized that the level of investment in yolk protein production might directly or indirectly trade off with immune capacity. First, we ask whether high levels of production of yolk proteins (YPs) in the fat body, occasioned by increased egg production, interferes with that same tissue’s ability to produce antimicrobial peptides (AMPs), the main effector molecules of the Drosophila immune system. In ongoing experiments, we are testing fertility and immune phenotypes of unmated or mated females with missense mutants in the three YP genes (Tanaka et al. 2021) and of null mutations in YP genes that we are generating with CRISPR-Cas9 genome editing. If removing YP production allows a higher immune response, we will test whether the SP-mediated increase in juvenile hormone (JH) levels in mated females is the basis for this tradeoff, as JH is known to stimulate YP production and decrease immune response. We will additionally test whether post-mating immune capacity is rescued by mutations that block early or late oogenesis. Together, these results can inform the mechanisms through which egg provisioning affects female immune response and generates a reproduction-immunity tradeoff.