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<p>Reproductive investment is frequently associated with compromised immune performance. In female <i>Drosophila melanogaster</i>, mating increases susceptibility to bacterial infections, and prior work has demonstrated that juvenile hormone (JH) signaling is necessary for this mating-induced reduction of immune performance. However, the temporal dynamics and key organ systems that mediate this JH-induced immunosuppression have not been studied. Here we show that post-mating sensitivity to bacterial infection depends on JH function spanning multiple life stages and target tissues. We find that mating induces a rapid, transient peak in JH titers and prolonged JH signaling activity. Transient treatment with exogenous JH is not sufficient to increase mortality from infection, suggesting continued JH activity is necessary for the persistent immune suppression observed after mating. Using conditional RNAi, we find that the JH receptor germ cells expressed (Gce) functions in the adipose tissue of developing pupae to potentiate post-mating sensitivity to infection in adults. In adult females, Gce appears to function in multiple tissues, including the fat body and ovary, to decrease infection resistance after mating. These results suggest that Gce function during metamorphic development sensitizes adult females to sustained JH signaling induced by mating. More broadly, our study illustrates how endocrine regulation of the interaction between development and reproduction can shape immune performance and infection outcome.</p>

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Juvenile hormone signaling acts during development and post-mating to suppress antibacterial defenses in Drosophila melanogaster

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年7月16日

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  • Scott A. Keith,
  • Vanika Gupta,
  • Ananda A. Kalukin,
  • Brian P. Lazzaro

摘要

Reproductive investment is frequently associated with compromised immune performance. In female Drosophila melanogaster, mating increases susceptibility to bacterial infections, and prior work has demonstrated that juvenile hormone (JH) signaling is necessary for this mating-induced reduction of immune performance. However, the temporal dynamics and key organ systems that mediate this JH-induced immunosuppression have not been studied. Here we show that post-mating sensitivity to bacterial infection depends on JH function spanning multiple life stages and target tissues. We find that mating induces a rapid, transient peak in JH titers and prolonged JH signaling activity. Transient treatment with exogenous JH is not sufficient to increase mortality from infection, suggesting continued JH activity is necessary for the persistent immune suppression observed after mating. Using conditional RNAi, we find that the JH receptor germ cells expressed (Gce) functions in the adipose tissue of developing pupae to potentiate post-mating sensitivity to infection in adults. In adult females, Gce appears to function in multiple tissues, including the fat body and ovary, to decrease infection resistance after mating. These results suggest that Gce function during metamorphic development sensitizes adult females to sustained JH signaling induced by mating. More broadly, our study illustrates how endocrine regulation of the interaction between development and reproduction can shape immune performance and infection outcome.