The TAO kinase KIN-18 regulates contractility and establishment of polarity in the C. elegans embryo


Fig. 7. Localization of KIN-­18 in the early embryo. (A) Staining of representative embryos of the indicated stage, and of a kin-­18(RNAi) embryo as control. Arrowheads indicate cortical KIN-­18, blue is DNA, white is KIN-­18 staining. (B) Fluorescence pictures of representative gfp::kin-­18 expressing embryos at one and two cells stage. (C) Cortical quantification of GFP::KIN-18 levels in, from the left, control, par-3(RNAi), par-2(RNAi), control and rho-1(RNAi) embryos. See materials and methods for the experimental settings. GFP::KIN-18 cortical levels are higher at the anterior cortex in both experiments (*p<0.05 and **p<0.001). In par mutants this asymmetry is lost. In par-2(RNAi) embryos, the increase in levels at anterior is not significantly different from the anterior in control embryos (p=0.39), while the increase in the posterior is significant (°p<0.02). The reduced KIN-18 anterior cortical levels in rho-1(RNAi) embryos is significant compared to anterior in control embryos (°°p<0.001), but anterior and posterior are still significantly different (+p<0.001) (PAR protein experiment: control RNAi n=21, par-3(RNAi) n=13 and par-2(RNAi) n=8; RHO-1 experiment: control RNAi n=14, rho-1(RNAi) n=19). Averages are shown, error bars represent s.e.m., scale bar 10 μm.

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