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Dauer morphogenesis requires inhibition of DBL-1-BMP signaling by ztf-30

ABSTRACT: In response to changing environments, the nematode C. elegans enters a stress-resistant diapause stage to survive adverse conditions. While the pathways controlling developmental arrest, such as insulin/ daf-2 and TGF-β/daf-7 are well characterized, mechanisms governing subsequent dauer morphogenesis remain poorly understood. Here, we report that the zinc-finger transcription factor ZTF-30 is dispensable for developmental arrest but essential for dauer morphogenesis. ztf-30 mutants form partial dauers that lack a protective thickened cuticle and specialized structures such as alae. Transcriptomics revealed that ztf-30 mutants precociously activate adult collagen expression and upregulate the DBL-1/BMP signaling pathway, which primarily modulates body size and innate immunity. These data suggest ZTF-30 represses BMP signaling. Consistent with this model, ztf-30 partial dauers show increased dbl-1 expression, increased DBL-1 signaling phenocopies ztf-30 loss, and reducing DBL-1 signaling rescues the partial dauer phenotype. During larval growth, ztf-30 loss causes ectopic hypodermal dbl-1 expression and increased body length. Ultimately, our findings establish that the active inhibition of DBL-1/BMP signaling is strictly required for proper dauer morphogenesis and we identify ZTF-30 as an essential transcriptional repressor driving this developmental shutdown.

ORGANISM(S): Caenorhabditis elegans

PROVIDER: GSE347961 | GEO | 2026/09/19

REPOSITORIES: GEO

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Project description:Post-embryonic development of the nematode C. elegans is governed by nutrient availability. 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. daf-16/FOXO had overlapping but distinct effects on gene expression in L1 arrest compared to daf-2/InsR adults. Notably, dbl-1/TGF-β, a ligand for the Sma/Mab pathway, and daf-36, which encodes an upstream component of the daf-12/NHR 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 and daf-36. 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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Dauer morphogenesis requires inhibition of DBL-1-BMP signaling by ztf-30

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