WormBase Tree Display for Interaction: WBInteraction000535987

WBInteraction000535987 Interaction_type: Genetic: Mutual_enhancement
    GI_module_one: Cis_phenotypic
    GI_module_two: Enhancing
    GI_module_three: Diverging
  Interactor: Interactor_overlapping_gene: WBGene00006868 Interactor_type: Non_directional
      WBGene00003111 Interactor_type: Non_directional
    Variation_interactor: WBVar00145253 Interactor_type: Non_directional
      WBVar00142901 Interactor_type: Non_directional
  Interaction_summary: vab-1(e2) and mab-20(ev574) mutually enhance each others embryonic lethal phenotype (Table S2). "The genetic interactions of plx-2 and mab-20 with vab-1 mutations in preventing pocket closure defects are more complex. For example, the vab-1 null mutation enhances both the plx-2 null and the mab-20 null synergistically for embryonic lethality (this enhancement is largely synthetic) (Figure 5C). By contrast, the kinase-deficient vab-1(e2) mutation enhances the embryonic lethality of the plx-2 null additively, if at all (Figure 5C), but enhances the mab-20 null synergistically. These results suggest that the kinase function of VAB-1 is redundant with the PLX-2-independent function of MAB-20, and the kinase-independent function of VAB-1 is redundant with the PLX-2-dependent function of MAB-20 in preventing pocket closure defects (see Figure 5D and Discussion)."
  Throughput: Low_throughput
  Interaction_phenotype: WBPhenotype:0000050
  Paper: WBPaper00040551
  Remark: Figure 5C, Table S2