期刊
GENETICS
卷 202, 期 1, 页码 175-+出版社
GENETICS SOCIETY AMERICA
DOI: 10.1534/genetics.115.182121
关键词
behavior; ecdysis; hormones; neural circuit; transgene targeting
资金
- Intramural Research Program of the National Institute of Mental Health
- FONDECYT [1141278]
- Centro Interdisciplinario de Neurociencia de Valparaiso [P09-022-F]
- Millennium Scientific Initiative of the Ministerio de Economia, Fomento y Turismo
- National Institutes of Health (NIH) grants from the National Institute of Neurological Disease and Stroke [R01NS021749]
- National Institute of Mental Health [R01MH067122]
- NATIONAL INSTITUTE OF MENTAL HEALTH [R01MH067122, ZIAMH002800] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE [R01NS021749] Funding Source: NIH RePORTER
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.
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