WormBase Tree Display for Interaction: WBInteraction000538566

WBInteraction000538566 Interaction_type: Genetic: Suppression
    GI_module_two: Suppressing
  Interactor: Interactor_overlapping_gene: WBGene00002173 Interactor_type: Effector
      WBGene00018488 Interactor_type: Affected
    Molecule_interactor: WBMol:00006000 Interactor_type: Affected
    Variation_interactor: WBVar00248962 Interactor_type: Effector
  Interaction_summary: "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)."
  Throughput: Low_throughput
  Interaction_RNAi: WBRNAi00110357
  Interaction_phenotype: WBPhenotype:0000050
  Paper: WBPaper00040893
  Remark: Fig. 6A