Fig 5. gsa-1(gf), acy-1(gf), and sphk-1(lf) mutations suppress fshr-1(lf) aldicarb phenotypes consistent with a downstream function.

Aldicarb paralysis and swimming assays were performed on wild type worms, fshr-1(ok778) mutants, and (A) gsa-1(ce81) or (B) acy-1(md1756) gain-of-function (gf) mutants, or (C) sphk-1(ok1097) loss-of-function mutants, along with their respective double mutants (gsa-1;fshr-1, acy-1;fshr-1, or sphk-1;fshr-1). (Left panels) Representative aldicarb assays showing the mean percentage of worms paralyzed on 1mM aldicarb ± s.e.m. for n = 3 plates of approximately 20 young adult animals each per strain. (Center panels) Bar graphs show cumulative data ± s.e.m. pooled from (A) 4 or (B) 8–9 independent aldicarb experiments for worms paralyzed at the timepoint indicated by an asterisk (*) in the upper panels. Scatter points show individual plate averages. Statistical significance of the data was analyzed using a Wilcoxon Rank Sum test followed by a Steel-Dwass multiple comparison analysis, as appropriate. Results of analyses for which p ≤ 0.05 are indicated by horizontal lines above the bars. (Right panels) Mean body bends per minute ± S.D. obtained in swimming experiments. Each scatter point represents an independent experiment testing 30 animals per genotype, analyzed by one-way ANOVA and Tukey’s post hoc test, *p ≤ 0.05, **p ≤ 0.01, ***p ≤ 0.0001, n.s., not significant.