Mutations in dpy-17 rescue mua-3(uy19) lethality. (A) Several suppressors were shown to suppress the mua-3 lethality. The P values were calculated by comparing the percent survival of each suppressor with that of the mua-3 mutants using the Student t test. (B) RNAi of dpy-17 rescued the mua-3 lethality, validating dpy-17 suppression of mua-3. (C) A model to suggest potential interactions among mua-3, dpy-17, and dpy-31 to regulate TGFβ signaling. Fibrillin-1, a human homolog of mua-3, sequesters TGFβ (DBL-1) to reduce the signal, whereas BMP-1/Tolloid metalloprotease (DPY-31) increases the signal. Based on the known interaction between DPY-17 and DPY-31 and its implication based on a function of DPY-31 homolog in mammals, it may be possible that the excess TGFβ (DBL-1) signal in the absence of MUA-3 could be ameliorated by reducing DPY-31 signal when DPY-17 was missing.