Growth and development of multicellular organisms are controlled by signaling systems that sense nutrition availability and metabolic status. We report a novel and surprising factor in Caenorhabditis elegans development, the monomethyl branched-chain fatty acid C17ISO, a product of leucine catabolism. We show here that C17ISO is an essential constituent in a novel mechanism that acts in parallel with the food-sensing DAF-2 (insulin receptor)/DAF-16 (FOXO) signaling pathway to promote post-embryonic development, and that the two pathways converge on a common target repressing cell cycle. We show that C17ISO homeostasis is regulated by a SREBP-1c-mediated feedback mechanism that is different from the SREBP-1c-mediated regulation of common fatty acid biosynthesis, as well as by peptide uptake and transport. Our data suggest that C17ISO may act as a chemical/nutritional factor in a mechanism that regulates post-embryonic development in response to the metabolic state of the organism. In Caenborhabditis elegans, environmental cues regulate the decision between two post-embryonic developmental options: reproductive growth and an adaptive larval arrest, known as diapause. There are two distinctive types of larval arrest, L1 (first larval stage) diapause and dauer formation (Johnson et al. 1984;Riddle and Alberts 1997;Muänoz 2003). Dauer larvae, third-stage larvae (dL3) with distinct structures and behaviors suited for long-term survival, are induced at the L1 larval stage by unfavorable growth conditions. The food-sensing insulin/DAF-2 receptor-stimulated pathway that negatively controls activity of a FOXO transcription factor, DAF-16, plays a critical role in dauer formation (Vowels and