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. 2018 Oct 17;9:4311. doi: 10.1038/s41467-018-06819-5

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© The Author(s) 2018

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 3 — Glutamate signaling from ASH to AIB mediates both quinine-induced reversal initiation and feeding suppression. a, b Both reversal initiation and feeding suppression induced by quinine were abolished in eat-4 mutant worms, and were dramatically declined in worms expressing eat-4 RNAi as a transgene in ASH. Specific expression of wild-type eat-4 gene in ASH partially rescued low-concentration quinine-induced reversal initiation, and fully restored high-concentration quinine-induced reversal initiation (a) and feeding suppression (b). Error bars: s.e.m. Reversal index, n = 6 groups, 10 worms/group at least; Pumping rate, n = 16 worms. ***p < 0.001 (t test or Wilcoxon test). c Calcium imaging shown that eat-4 is required for quinine-induced calcium elevation in AIB. Left: average trace. The shades around traces indicate error bars (s.e.m.). n ≥ 14. **p < 0.01 (t test)