Abstract
In response to adverse environmental conditions many organisms from nematodes to mammals deploy a dormancy strategy, causing states of developmental or reproductive arrest that enhance somatic maintenance and survival ability at the expense of growth or reproduction. Dormancy regulation has been studied in C. elegans and in several insects, but how neurosensory mechanisms act to relay environmental cues to the endocrine system in order to induce dormancy remains unclear. Here we examine this fundamental question by genetically manipulating aminergic neurotransmitter signaling in Drosophila melanogaster. We find that both serotonin and dopamine enhance adult ovarian dormancy, while the downregulation of their respective signaling pathways in endocrine cells or tissues (insulin producing cells, fat body, corpus allatum) reduces dormancy. In contrast, octopamine signaling antagonizes dormancy. Our findings enhance our understanding of the ability of organisms to cope with unfavorable environments and illuminate some of the relevant signaling pathways.
Highlights
Dormancy is a widespread phenotypically plastic response that enables organisms – both vertebrates and invertebrates – to survive adverse environmental conditions[1,2,3]
Our results demonstrate that both serotonin and dopamine promote ovarian dormancy by relaying dormancy-inducing cues to major endocrine sites known to be central for dormancy physiology, including the IPCs, CA and fat body
Since dILPs act as dormancy antagonists[14,15], and because the production of dILPs by the IPCs is inhibited by the serotonin receptor[48,49], we first asked whether manipulating serotonin receptor levels in the IPCs affects dormancy
Summary
Dormancy is a widespread phenotypically plastic response that enables organisms – both vertebrates and invertebrates – to survive adverse environmental conditions[1,2,3]. In fruit flies (Drosophila) and other insects, adult females enter ovarian dormancy by arresting gonadal maturation in response to cold (
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