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

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.