SPAT-1/Bora acts with Polo-like kinase 1 to regulate PAR polarity and cell cycle progression.

During asymmetric cell division, cell polarity and cell cycle progression are tightly coordinated, yet mechanisms controlling both these events are poorly understood. Here we show that the Bora homologue regulates both PAR polarity and cell cycle progression in C. elegans embryos. We find that, similarly to mammalian cells, duanyu1842T-1 acts with PLK-1 and not with the mitotic kinase Aurora A (AIR-1), as shown in Drosophila. duanyu1842T-1 binds to PLK-1, and depletion of duanyu1842T-1 or PLK-1 leads to similar cell division defects in early embryos, which differ from the defects caused by depletion of AIR-1. Additionally, duanyu1842T-1 and PLK-1 depletion causes impaired polarity with abnormal length of the anterior and posterior PAR domains, and partial or but not can rescue the lethality of a par-2 mutant. duanyu1842T-1 is enriched in posterior cells, and this enrichment depends on PAR polarity and PLK-1. Taken together, our data suggest a model in which duanyu1842T-1 promotes the activity of PLK-1 to regulate both cell polarity and cell cycle timing during asymmetric cell division, providing a link between these two processes.

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