title: Juvenile Hormone Suppresses Resistance to Infection in Mated Female Drosophila melanogaster.
abstract: Hormonal signaling provides metazoans with the ability to regulate development, growth, metabolism, immune defense, and reproduction in response to internal and external stimuli. The use of hormones as central regulators of physiology makes them prime candidates for mediating allocation of resources to competing biological functions (i.e., hormonal pleiotropy) [1]. In animals, reproductive effort often results in weaker immune responses (e.g., [2-4]), and this reduction is sometimes linked to hormone signaling (see [5-7]). In the fruit fly, Drosophila melanogaster, mating and the receipt of male seminal fluid proteins results in reduced resistance to a systemic bacterial infection [8, 9]. Here, we evaluate whether the immunosuppressive effect of reproduction in female D. melanogaster is attributable to the endocrine signal juvenile hormone (JH), which promotes the development of oocytes and the synthesis and deposition of yolk protein [10, 11]. Previous work has implicated JH as immunosuppressive [12, 13], and the male seminal fluid protein Sex Peptide (SP) activates JH biosynthesis in female D. melanogaster after mating [14]. We find that transfer of SP activates synthesis of JH in the mated female, which in turn suppresses resistance to infection through the receptor germ cell expressed (gce). We find that mated females are more likely to die from infection, suffer higher pathogen burdens, and are less able to induce their immune responses. All of these deficiencies are rescued when JH signaling is blocked. We argue that hormonal signaling is important for regulating immune system activity and, more generally, for governing trade-offs between physiological processes.
authors.affiliation: Field of Genetics, Genomics, and Development, Cornell University, Ithaca, NY 14853, USA; Department of Entomology, Cornell University, Ithaca, NY 14853, USA; Cornell Institute of Host-Microbe Interactions and Disease, Cornell University, Ithaca, NY 14853, USA. Electronic address: ras599@cornell.edu.
authors.forename: Robin A
authors.initials: RA
authors.lastname: Schwenke
authors.affiliation: Field of Genetics, Genomics, and Development, Cornell University, Ithaca, NY 14853, USA; Department of Entomology, Cornell University, Ithaca, NY 14853, USA; Cornell Institute of Host-Microbe Interactions and Disease, Cornell University, Ithaca, NY 14853, USA. Electronic address: bplazzaro@cornell.edu.
authors.forename: Brian P
authors.initials: BP
authors.lastname: Lazzaro
mesh_terms: D000818:Animals; D029721:Drosophila Proteins / Q000378:metabolism; D004331:Drosophila melanogaster / Q000276:immunology / Q000502:physiology*; D005260:Female; D007108:Immune Tolerance / Q000276:immunology*; D036341:Intercellular Signaling Peptides and Proteins; D007605:Juvenile Hormones / Q000378:metabolism*; D010455:Peptides / Q000378:metabolism; D012098:Reproduction / Q000276:immunology; D012726:Sexual Behavior, Animal
chemical_list: D029721:Drosophila Proteins; D036341:Intercellular Signaling Peptides and Proteins; D007605:Juvenile Hormones; D010455:Peptides; C056736:SP protein, Drosophila
keywords: endocrine; evolution; hormone; immune defense; insect immunity; mating; providencia; reproduction; trade-off; tradeoff