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)."