RNAi knockdown of <i>C</i>. <i>elegans</i> kinases results in variable effects on vulva development, while knockdown of <i>C</i>. <i>elegans</i> phosphatases results in more uniform effects.

<p>A. Illustration of the experimental pipeline. Age-synchronized animals were grown on kinase/phosphatase specific RNAi-expressing bacteria at the indicated conditions. The percentage of animals showing a disrupted vulva development (Multivulva / Vulvaless) was scored at day 2 of adulthood. B. For each RNAi-treatment of a kinase (or phosphatase) in animals with perturbed RAS signaling, the percentage of animals with disrupted vulva phenotype was scored. Shown are the medians (± SEM) of at least 3 independent experiments. Four kinase treatments and two phosphatase treatments showed a significantly higher tendency for disrupted phenotype relative to control (p-values: <i>mpk-1</i> p = 0.012, F31E3.2 p = 0.024, <i>mek-2</i> p = 0.024, <i>lin-2</i> p = 0.02, <i>ptp-2</i> p = 4*10⁻³, <i>dep-1</i> p = 0.046; Mann-Whitney test). C. Same as in B, for animals with perturbed wnt/beta-catenin signaling. Five kinase treatments and four phosphatase treatments showed a significantly higher tendency for disrupted phenotype relative to control (p-values: <i>lin-2</i> p = 2.2*10⁻³, mek-2 p = 0.013, <i>par-1</i> p = 0.018, <i>mpk-1</i> p = 0.043, <i>pkc-3</i> p = 8.6*10⁻³, <i>let-92</i> p = 4.6*10⁻³, <i>dep-1</i> p = 0.017, <i>ptp-2</i> p = 0.027, <i>eya-1</i> p = 0.023; Mann-Whitney test).