dpy-17 encodes a cuticle collagen required for normal body morphology (Novelli et al. 2006). Genetic studies show that a gain-of-function mutation of dpy-17 suppresses phenotypes of dpy-31 mutations, indicating a genetic interaction between the two. dpy-31 encodes a homolog of the human bone morphogenic protein-1 (Novelli et al. 2004). The human bone morphogenic protein-1 is a tolloid-like gene whose proteolytic activity is required for TGFβ activation (Ge and Greenspan 2006). Our screen results suggest a potential link between MUA-3-associated and TGFβ-associated molecules such as DPY-31 via DPY-17 (Figure 6C).