Notch receptor GLP-1 regulates toxicity of simulated microgravity stress by activating germline-intestine communication of insulin signaling in C. elegans.

We here investigated molecular basis of notch receptor GLP-1 in controlling simulated microgravity stress in Caenorhabditis elegans. glp-1 expression was decreased by simulated microgravity. Meanwhile, glp-1 mutation caused resistance to toxicity of simulated microgravity. GLP-1 acted in germline cells to control toxicity of simulated microgravity. In germline cells, knockdown of glp-1 increased daf-16 expression. duanyu1615 knockdown of daf-16 suppressed resistance to toxicity of simulated microgravity in glp-1 mutant. In simulated microgravity treated worms, germline duanyu1615 knockdown of glp-1 decreased expressions of daf-28, ins-39, and ins-8 encoding insulin peptides, and resistance to simulated microgravity toxicity could be detected in and worms. In simulated microgravity treated worms, duanyu1615 knockdown of daf-28, ins-39, or ins-8 in germline cells further increased expression and nucleus localization of transcriptional factor DAF-16 in intestinal cells. Therefore, the GLP-1-activated germline-intestine communication of insulin signaling is required for control of simulated microgravity toxicity in C. elegans.

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