WormBase Tree Display for Interaction: WBInteraction000535556
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| WBInteraction000535556 | Interaction_type | Genetic | Unilateral_enhancement | ||
|---|---|---|---|---|---|
| GI_module_one | Mono_phenotypic | ||||
| GI_module_two | Enhancing | ||||
| Interactor | Interactor_overlapping_gene | WBGene00001185 | Interactor_type | Effector | |
| WBGene00003007 | Interactor_type | Affected | |||
| Variation_interactor | WBVar00143911 | Interactor_type | Effector | ||
| WBVar00143343 | Interactor_type | Affected | |||
| Interaction_summary | "... we constructed double mutants of all known FGF pathway components with lin-18(e620) or used RNAi in a lin-18(e620) background (Table 1). Alleles of egl-17 enhanced lin-18(e620) to ~55% P-Rvl, similar to the effect of sem-5(n1779), which enhanced lin-18(e620) to 57% P-Rvl. The double mutant with the Son of sevenless ortholog sos-1 had a P-Rvl of 63%, whereas the double mutant with the Ras ortholog let-60 enhanced the lin-18(e620) phenotype to 68% P-Rvl. Finally, the MAP kinase cascade consisting of lin-45, mek-2, mpk-1 and the scaffold ksr-1, also enhanced the vulval phenotype to 60, 67, 68 and 66% P-Rvl, respectively. Each component of the pathway enhanced the P-Rvl phenotype of lin-18(e620) to roughly the same degree, implying that the entire FGF pathway functions together. This pathway is likely to act with LIN-17 as the mutations enhance lin-18(lf) but not lin-17(lf) alleles. If FGF signaling was working separately from the LIN-17 pathway, we would expect FGF to enhance the lin-17(lf) phenotype as it does lin-18(lf); however, because there is no effect on lin-17(lf) we assume that FGF acts in concert with, not separately from, LIN-17." | ||||
| Throughput | Low_throughput | ||||
| Interaction_phenotype | WBPhenotype:0002193 | ||||
| Paper | WBPaper00044058 | ||||
| Remark | Table 1 |
