"... 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."