Some of small peptides function as primary neurotransmitters through their receptors in diverse species of animals. C. elegans also has many of small neuropeptides and their receptors predicted by the genome sequence. Our screen for neuropeptide receptors (NPRs) relevant to dauer arrest revealed that disruption of
npr-17 drastically reduced dauer arrest induced by dauer pheromones. NPR-17 is a GPCR and expressed in the ASI neurons and intestine. It has been reported that NPR-17 is a receptor of the neuropeptides, NLP-3 and NLP-24, which regulate withdrawal from noxious chemical stimuli (1). Interestingly, disruption of
nlp-3 reduced dauer arrest, similar to that of
npr-17, whereas that of
nlp-24 did not. To elucidate molecular mechanism of NPR-17 on modulation of dauer arrest, we first carried out epistasis analysis on TGF-b-like and insulin-like signaling pathways.
daf-7 and
daf-2 are epistatic to
npr-17. Next, we investigated relevance of NPR-17 to secretion of a TGF- beta , DAF-7, and an insulin-like peptide, DAF-28, which are produced in the ASI neurons and regulate larval growth. In a
npr-17(-) background, accumulation of DAF-7::mCherry in coelomocytes increased, while that of DAF-28::mCherry did not. In addition, we also investigated secretion of an insulin-like peptide, INS-35, which is mainly produced in intestine (2). In a
npr-17(-) background, accumulation of INS-35::VENUS in coelomocytes scarcely increased. Together, these results suggest that NPR-17 promotes dauer arrest by suppressing secretion of DAF-7, not of insulin-like peptides, DAF-28 and INS-35. (1) Mils, H., et al. J Neurosci. 36:5498 (2016). (2) Matsunaga, Y., et al. Nat. Commun. 7:10573 (2016).