Fig. 2. Achieving PLK-1 asymmetry. (A-D) Wild-type (A), zen-4(RNAi) (B), tba-2(RNAi) (C) or nmy-2(RNAi) (D) embryos stained for PLK-1 (shown alone in the left panels and in red in the merged panels), -tubulin (green) and DNA (blue). PLK-1 asymmetry is maintained despite cytokinesis failure (B). Whereas microtubules are not essential for PLK-1 asymmetry as the asymmetry is maintained and even slightly increased upon -tubulin depletion (C), the actomyosin network is needed (D). (E,F) Wild-type (E) and partial plk-1(RNAi) (F) embryos stained for PLK-1 (shown alone in the left panels and in red in the merged panels), -tubulin (green) and DNA (blue). Overall PLK-1 levels are diminished in partial plk-1(RNAi) embryos (F, top panel). To better illustrate the alteration in ratio between AB and P₁, a second image of the same partial plk-1(RNAi) embryo is shown (F, bottom panel), in which intensities were increased so as to match those in AB in the wild-type embryo. (G) Average ratios, along with s.e.m., of PLK-1 in AB versus P₁ in wild-type and partial plk-1(RNAi) embryos stained as in E and F. Wild type, 1.52±0.05, n=64; partial plk-1(RNAi), 1.97±0.13, n=16. Student's t-test, P=2.6x10^-11. The star indicates that the difference with wild type is statistically significant.