C. elegans dauer morphogenesis requires inhibition of DBL-1/BMP signaling by ztf-30.

Abstract

In response to changing environments, the nematode Caenorhabditis 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, zt-f-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.