WormBase Tree Display for Interaction: WBInteraction000535985
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| WBInteraction000535985 | Interaction_type | Genetic | Unilateral_enhancement | ||
|---|---|---|---|---|---|
| GI_module_one | Mono_phenotypic | ||||
| GI_module_two | Enhancing | ||||
| Interactor | Interactor_overlapping_gene | WBGene00004048 | Interactor_type | Effector | |
| WBGene00006868 | Interactor_type | Affected | |||
| Variation_interactor | WBVar00145286 | Interactor_type | Effector | ||
| WBVar00142887 | Interactor_type | Affected | |||
| Interaction_summary | plx-2(ev773) enhances the embryonic lethality of vab-1(dx31) mutants (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)... The pattern of redundancies governing prevention of lethality (last four gray data bars to the right in Figure 5C) is nearly identical to the pattern of redundancies governing the prevention of gaps between sister plexin band cells (last four black data bars to the right in Figure 5B). This strongly suggests that the synergistic enhancement of vab-1 mutant embryonic lethality by plx-2 mutations is caused by the persistence of gaps between sister plexin band cells, which block migrating P9/10 cells from completing pocket closure. This interpretation is supported by cell-type-specific rescue data presented below and considered further in the Discussion." | ||||
| Throughput | Low_throughput | ||||
| Interaction_phenotype | WBPhenotype:0000050 | ||||
| Paper | WBPaper00040551 | ||||
| Remark | Figure 5C, Table S2 |
