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. 2018 Feb 1;32(3-4):258–270. doi: 10.1101/gad.309625.117

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© 2018 Zhang et al.; Published by Cold Spring Harbor Laboratory Press

This article is distributed exclusively by Cold Spring Harbor Laboratory Press for the first six months after the full-issue publication date (see http://genesdev.cshlp.org/site/misc/terms.xhtml). After six months, it is available under a Creative Commons License (Attribution-NonCommercial 4.0 International), as described at http://creativecommons.org/licenses/by-nc/4.0/.

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Figure 1. — The cool-sensitive IL1 neurons signal the intestine to extend life span at lower temperatures. (A,B) trpa-1 mutant worms are short-lived at lower but not higher temperatures, and transgenic expression of TRPA-1 in neurons extends life span at lower but not higher temperatures. The pan-neuronal promoter Prgef-1 was used to drive expression of TRPA-1 as a transgene in neurons. (C) Transgenic expression of TRPA-1 in sensory neurons extends life span at lower temperatures. The pan-sensory neuron promoter Posm-6 was used to drive expression of TRPA-1 as a transgene in sensory neurons. (D) Transgenic expression of TRPA-1 in motor neurons and a group of interneurons does not extend life span. The acr-2 and unc-25 promoter drives expression in cholinergic and GABAergic motor neurons, respectively, while the glr-1 promoter directs expression in interneurons. (E,F) Transgenic expression of TRPA-1 in IL1 neurons extends life span at lower (E) but not higher (F) temperatures. A segment of aqp-6 promoter was used to drive expression specifically in IL1 neurons. (G) Transgenic expression of TRPA-1 in IL1 neurons is sufficient to rescue the short-lived phenotype of trpa-1 mutant worms at lower temperatures. (H–J) IL1 neurons are cool-sensitive and depend on TRPA-1 for cool sensation. The genetically encoded calcium sensor GCaMP6(f) was expressed as a transgene in IL1 neurons. DsRed was coexpressed as an internal reference marker to enable ratiometric imaging. While IL1 neurons did not respond to warming (H), cooling evoked robust calcium transients in these neurons (I). Shades along the traces in H and I represent error bars (SEM). Bar graphs in J summarize the data in I. n ≥ 7. (**) P < 0.005, ANOVA with Bonferroni test. (K) Blocking the output of IL1 neurons shortens life span at lower temperatures. Tetanus toxin (TeTx) was expressed as a transgene in IL1 neurons to block the exocytosis from IL1 neurons. (L) Enhancing the output of IL1 neurons extends life span. The gain-of-function form of Drosophila syntaxin, known to promote exocytosis, was expressed in IL1 neurons as a transgene to enhance the output from IL1 neurons. (M) Extension of life span by IL1 neurons requires DAF-16. Loss of DAF-16 blocked the life span-extending effect of IL1 neurons. (N,O) DAF-16 acts in the intestine instead of neurons to mediate the life span-extending effect of IL1 neurons. daf-16 cDNA expressed as a transgene in the intestine using the ges-1 promoter rescued the phenotype of daf-16 mutant worms (N), while its expression in neurons using the rgef-1 promoter did not (O).