ArticlePLoS genetics2015
dbl-1/TGF-β and daf-12/NHR Signaling Mediate Cell-Nonautonomous Effects of daf-16/FOXO on Starvation-Induced Developmental Arrest.
Article in PLoS genetics, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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41 citing papers in PubMed, 66 citations in OpenAlex.
- An atlas of thebioRxiv : the preprint server for biology · 2026Article
- Nutrient-responsive and DAF-16/FoxO target H1 histone HIL-1 promotes resistance to starvation and bacterial pathogens inbioRxiv : the preprint server for biology · 2026Article
- Three muscle-specific DAF-16/FOXO transcriptional targets activated by reduced insulin/IGF-1 signaling.G3 (Bethesda, Md.) · 2026Article
- Transcriptome- and phenotype-based epistasis analysis in Caenorhabditis elegans reveals daf-16/FoxO-dependent and independent effects of daf-2/InsR in L1 starvation and recovery.G3 (Bethesda, Md.) · 2026Article
- Short-term L1 arrest duration does not significantly alter organismal phenotypes in synchronizedmicroPublication biology · 2026Article
- Systematic optimization ofBiochemistry and biophysics reports · 2025Article
- Early life starvation and Hedgehog-related signaling activate innate immunity downstream of daf-18/PTEN and lin-35/Rb causing developmental pathology in adult C. elegans.PLoS genetics · 2025Article
- DAF-18/PTEN protects LIN-35/Rb from CLP-1/CAPN-mediated cleavage to promote starvation resistance.Life science alliance · 2025Article
- Free long-chain fatty acids trigger early postembryonic development in starved Caenorhabditis elegans by suppressing mTORC1.PLoS biology · 2024Article
- Germline loss in C. elegans enhances longevity by disrupting adhesion between niche and stem cells.The EMBO journal · 2024Article
- Regulatory mechanism of cold-inducible diapause in Caenorhabditis elegans.Nature communications · 2024Article
- Inhibiting HSD17B8 suppresses the cell proliferation caused by PTEN failure.Scientific reports · 2024Article
- Inhibition of ribosome biogenesis in the epidermis is sufficient to trigger organism-wide growth quiescence independently of nutritional status in C. elegans.PLoS biology · 2023Article
- Article
- TGF-β pathways in aging and immunity: lessons fromFrontiers in genetics · 2023Review
- Mitochondrial genome recovery by ATFS-1 is essential for development after starvation.Cell reports · 2022Article
- Alternative somatic and germline gene-regulatory strategies during starvation-induced developmental arrest.Cell reports · 2022Article
- Reduced bone morphogenic protein signaling along the gut-neuron axis by heat shock factor promotes longevity.Aging cell · 2022Article
- Genetic analysis of daf-18/PTEN missense mutants for starvation resistance and developmental regulation during Caenorhabditis elegans L1 arrest.G3 (Bethesda, Md.) · 2022Article
- Flavonol glycoside complanatoside A requires FOXO/DAF-16, NRF2/SKN-1, and HSF-1 to improve stress resistances and extend the life span ofFrontiers in pharmacology · 2022Article
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7 authors at 1 institution in 1 country.
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Abstract
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.
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