| Literature DB >> 28439025 |
Matthew Meiselman1,2,3, Sang Soo Lee1,2,4, Raymond-Tan Tran1,2, Hongjiu Dai1,2, Yike Ding1, Crisalejandra Rivera-Perez5, Thilini P Wijesekera6, Brigitte Dauwalder6, Fernando Gabriel Noriega5, Michael E Adams7,2,3,4.
Abstract
Ecdysis-triggering hormone (ETH) was originally discovered and characterized as a molt termination signal in insects through its regulation of the ecdysis sequence. Here we report that ETH persists in adult Drosophila melanogaster, where it functions as an obligatory allatotropin to promote juvenile hormone (JH) production and reproduction. ETH signaling deficits lead to sharply reduced JH levels and consequent reductions of ovary size, egg production, and yolk deposition in mature oocytes. Expression of ETH and ETH receptor genes is in turn dependent on ecdysone (20E). Furthermore, 20E receptor knockdown specifically in Inka cells reduces fecundity. Our findings indicate that the canonical developmental roles of 20E, ETH, and JH during juvenile stages are repurposed to function as an endocrine network essential for reproductive success.Entities:
Keywords: ecdysis triggering hormone; ecdysone; fecundity; juvenile hormone; oogenesis
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Year: 2017 PMID： 28439025 PMCID： PMC5441734 DOI： 10.1073/pnas.1620760114
Source DB: PubMed Journal: Proc Natl Acad Sci U S A ISSN： 0027-8424 Impact factor: 11.205