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Fig. 7. PLK-1 mediated differential timing is independent of ATL-1. (A-C) Wild-type (A), atl-1(tm853) (B) or div-1(RNAi) (C) two-cell stage embryo stained for PLK-1 (shown alone in left panels and in red in the merged panels), -tubulin (green) and DNA (blue). PLK-1 distribution is asymmetric as in the wild type. (D) Average ratios, along with s.e.m., of PLK-1 in AB versus P₁ determined on fixed wild-type, atl-1(tm853) and div-1(RNAi) embryos. Wild type, 1.52±0.05, n=64; atl-1(tm853), 1.48±0.12, n=9, P=0.58, compared with the wild type (two-tailed Student's t-test); div-1(RNAi), 1.45±0.17, n=8, P=0.32, compared with the wild type (two-tailed Student's t-test). (E-G) Images from DIC time-lapse microscopy of wild-type (E), atl-1(tm853) (F) or atl-1(tm853) embryos treated with mild plk-1(RNAi) (G) (see corresponding Movies 5, 9-10 in the supplementary material). See legend of Fig. 5 for explanation of symbols and timing. (H) Average ratios ±s.e.m. of the duration of interphase in P₁ over the duration of interphase in AB [(I_P1)/(I_AB)] (RI) in embryos of the indicated genotypes. The star denotes that the difference with wild type is statistically significant. See Table S2 in the supplementary material for numerical values and statistical analysis. (I) Working model. Preferential promotion of mitotic entry in AB through the presence of more PLK-1, together with preferential retardation of mitotic entry in P₁ through engagement of an ATL-1/CHK-1-dependent checkpoint, ensure differential cell cycle duration in two-cell stage C. elegans embryos.

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