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Nutrient availability has profound influence on development. In the nematode  C .  elegans , nutrient availability governs post-embryonic development. L1-stage larvae remain in a state of developmental arrest after hatching until they feed. This “L1 arrest” (or "L1 diapause") is associated with increased stress resistance, supporting starvation survival. Loss of the transcription factor  daf-16 /FOXO, an effector of insulin/IGF signaling, results in arrest-defective and starvation-sensitive phenotypes. We show that  daf-16 /FOXO regulates L1 arrest cell-nonautonomously, suggesting that insulin/IGF signaling regulates at least one additional signaling pathway. We used mRNA-seq to identify candidate signaling molecules affected by  daf-16 /FOXO during L1 arrest.  dbl-1 /TGF-β, a ligand for the Sma/Mab pathway,  daf-12 /NHR and  daf-36 /oxygenase, an upstream component of the  daf-12  steroid hormone signaling pathway, were up-regulated during L1 arrest in a  daf-16 /FOXO mutant. Using genetic epistasis analysis, we show that  dbl-1 /TGF-β and  daf-12 /NHR steroid hormone signaling pathways are required for the  daf-16 /FOXO arrest-defective phenotype, suggesting that  daf-16 /FOXO represses  dbl-1 /TGF-β,  daf-12 /NHR and  daf-36 /oxygenase. The  dbl-1 /TGF-β and  daf-12 /NHR pathways have not previously been shown to affect L1 development, but we found that disruption of these pathways delayed L1 development in fed larvae, consistent with these pathways promoting development in starved  daf-16 /FOXO mutants. Though the  dbl-1 /TGF-β and  daf-12 /NHR pathways are epistatic to  daf-16 /FOXO for the arrest-defective phenotype, disruption of these pathways does not suppress starvation sensitivity of  daf-16 /FOXO mutants. This observation uncouples starvation survival from developmental arrest, indicating that DAF-16/FOXO targets distinct effectors for each phenotype and revealing that inappropriate development during starvation does not cause the early demise of  daf-16 /FOXO mutants. Overall, this study shows that  daf-16 /FOXO promotes developmental arrest cell-nonautonomously by repressing pathways that promote larval development.

dbl-1/TGF-β and daf-12/NHR Signaling Mediate Cell-Nonautonomous Effects of daf-16/FOXO on Starvation-Induced Developmental Arrest