"We then investigated whether a potential failure of IP3 signaling could cause the
acs-1(RNAi)C17ISO Emb phenotype. If IP3 production at the plasma membrane in
acs-1(RNAi)C17ISO embryos is reduced, then raising the level of IP3 or enhancing the sensitivity of the IP3 receptor may rescue the Emb phenotype. To test this hypothesis, we carried out a genetic analysis using a loss-of-function (lf) mutation in
ipp-5 (encoding a type I phosphatase that converts IP3 to inositol 1,4 bisphosphate [IP2]) and a gain-of-function (gf) mutation in the only IP3 receptor gene,
itr-1 (Clandinin et al. 1998; Baylis et al. 1999; Dal Santo et al. 1999; Bui and Sternberg 2002). Specifically, mutants and wild-type controls were treated with
acs-1(RNAi) in the presence or absence of C17ISO supplementation (Supplemental Fig. S5). We found that Emb was suppressed in both mutants with hyperactive IP3 signaling (Fig. 6A)."