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

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Fig. 10. KIN-18 plays a role in polarity establishment. (A) Schematic representation of polarity establishment (before PNM) and polarity maintenance phases (after PNM, and after pseudocleavage relaxation for kin-­18(RNAi)) in the indicated genotypes. PAR-­6 is depicted in blue, PAR-­2 in red, cortex devoid of both PAR-­6 and PAR-­2 is in black. Thickness and darkness of the lines reflect abundance or activity of the indicated protein. (B)­par-­2(it5ts) embryonic lethality suppression by RNAi depletion of the indicated genes. Depletion of PAR-6, KIN-18 or DIV-1 all significantly suppress par-2(it5ts) lethality (*p<0.001 with respect to par-­2(it5ts) in control RNAi). In these conditions, par-6(RNAi) results in weak lethality in wild type embryos (°p500 embryos were counted. Note that the levels of suppression of par-2(it5ts) lethality vary between the different RNAi. This might depend on the mechanism exerted by the gene in the system, but as well as on the specific RNAi penetrance and the balance between toxic/favorable effects of each combination. For instance par-3(RNAi) or pkc-3(RNAi) is less efficient than par-6(RNAi) to rescue par-2(it5ts) lethality, although they should in principle impinge on the same pathway.

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