Rescue of <i>fshr-1</i> neuromuscular defects by additional independent <i>fshr-1</i> transgenes.

<p>Aldicarb paralysis assays and swimming assays were performed on wild type worms, <i>fshr-1(ok778)</i> mutants, and rescued animals re-expressing <i>fshr-1</i> under either (A) the endogenous <i>fshr-1</i> promoter (P<i>fshr-1</i>, <i>fdEx41</i>), (B) an intestinal promoter (P<i>ges-1</i>, <i>agIs35</i>) or (C) a pan-neuronal promoter (P<i>ric-19</i>, <i>agEx52</i>) in the <i>fshr-1</i> mutant background. (A-B) (<i>Left panels</i>) Representative aldicarb assays showing the percentage of worms paralyzed on 1mM aldicarb ± s.e.m. for n = 3 plates of approximately 20 young adult animals each per strain. (<i>Center panels</i>) Bar graphs showing cumulative data ± s.e.m. pooled from 3–4 independent experiments for worms paralyzed at the timepoint indicated by an asterisk (*) in the upper panels. Scatter points show individual plate averages. (<i>Right panels</i>) Box and whisker plots showing mean body bends per minute from swimming assays performed on n = 30 young adult animals of each genotype. Statistical significance of the data was analyzed using a one-way ANOVA and Tukey’s post hoc test or a Wilcoxon Rank Sum test followed by a Steel-Dwass multiple comparison analysis, as appropriate. Results of analyses for which <i>p</i> ≤ 0.05 are indicated by horizontal lines above the bars. <i>*p</i> ≤ 0.05, **<i>p</i> ≤ 0.01, <i>***p</i> ≤ 0.0001.</p> <p>(PDF)</p>