Fig. 4

SSU-1 and DAF-16 regulate lysophosphatidylcholine levels in response to osmotic stress. a Relative levels of polar metabolites exhibiting a statistically significant (p < 0.01) change in levels in ssu-1(fc73) and daf-16(m26) mutant embryos. Metabolites were normalized to the levels of histidine. n = 3 replicates. Error bars, s.d. b Relative levels of lipid metabolites exhibiting a statistically significant (p < 0.01 two-tailed t-test) change in levels in both ssu-1(fc73) and daf-16(m26) mutant embryos. Metabolites were normalized to the levels of total lipid. n = 3 replicates. Error bars, s.d. PC phosphatidylcholine, AcCa acylcarnitine, PE phosphatidylethanolamine, TG triglyceride. c Relative levels of lysophosphatidylcholine (LPC) metabolites in the wild-type and ssu-1(fc73) and daf-16(m26) mutant embryos. Metabolites shown exhibited a statistically significant (p < 0.01 two-tailed t-test) and greater than twofold increase in abundance in response to osmotic stress (300 mM NaCl) and required both SSU-1 and DAF-16. Metabolites were normalized to the levels of total lipid. n = 3 replicates. Error bars, s.d. d Percent of wild-type embryos from parents fed 1 mM lysophosphatidylcholines (LPCs) that hatch. Error bars, s.d. e Diagram of the genetic pathway regulating C. elegans development in response to osmotic stress. This diagram is based on the results described here and the insulin-like signaling pathway regulating developmental arrest in response to osmotic stress described previously by Burton et al.⁵. f Model for how C. elegans regulates development in response to osmotic stress. This model is based on the results described here and the results described previously by Burton et al.⁵ Source data are provided as a Source Data file