The splice isoforms of the Drosophila ecdysis triggering hormone receptor have developmentally distinct roles

Feici Diao, Wilson Mena, Jonathan Shi, Dongkook Park, Fengqiu Diao, Paul Taghert, John Ewer, Benjamin H. White

Research output: Contribution to journalArticlepeer-review

25 Scopus citations

Abstract

To grow, insects must periodically shed their exoskeletons. This process, called ecdysis, is initiated by the endocrine release of Ecdysis Trigger Hormone (ETH) and has been extensively studied as a model for understanding the hormonal control of behavior. Understanding how ETH regulates ecdysis behavior, however, has been impeded by limited knowledge of the hormone’s neuronal targets. An alternatively spliced gene encoding a G-protein-coupled receptor (ETHR) that is activated by ETH has been identified, and several lines of evidence support a role in ecdysis for its A-isoform. The function of a second ETHR isoform (ETHRB) remains unknown. Here we use the recently introduced “Trojan exon” technique to simultaneously mutate the ETHR gene and gain genetic access to the neurons that express its two isoforms. We show that ETHRA and ETHRB are expressed in largely distinct subsets of neurons and that ETHRA- but not ETHRB-expressing neurons are required for ecdysis at all developmental stages. However, both genetic and neuronal manipulations indicate an essential role for ETHRB at pupal and adult, but not larval, ecdysis. We also identify several functionally important subsets of ETHR-expressing neurons including one that coexpresses the peptide Leucokinin and regulates fluid balance to facilitate ecdysis at the pupal stage. The general strategy presented here of using a receptor gene as an entry point for genetic and neuronal manipulations should be useful in establishing patterns of functional connectivity in other hormonally regulated networks.

Original languageEnglish
Pages (from-to)175-189
Number of pages15
JournalGenetics
Volume202
Issue number1
DOIs
StatePublished - Jan 2016

Keywords

  • Behavior
  • Ecdysis
  • Hormones
  • Neural circuit
  • Transgene targeting

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