Cell polarity is established in Caenorhabditis elegans by segregating conserved Partitioning defective (PAR) proteins to the opposite sides of the cell during asymmetric cell division to specify cell fate. The mitotic kinase Aurora A (AIR-1) has been shown to regulate the anterior-posterior polarity in C. elegans zygotes, but the underlying mechanism is still unclear. Here, Daniel Dickinson and colleagues find that acute and chronic inactivation of AIR-1 produce opposite polarity phenotypes in C. elegans zygotes. The authors first observe that AIR-A depletion with RNAi or kinase inhibitors show distinct polarity phenotypes. Then, using an auxin-inducible degradation system to deplete AIR-1 at different times of the cell cycle, the authors find that AIR-1 regulates PAR protein localization differently at different stages. Specifically, AIR-1 prevents bipolarity in meiosis I and, later in the cell cycle, it is required to load PAR proteins to the posterior end for symmetry breaking. Furthermore, the authors use an inhibitor to inactivate Polo-like kinase (PLK-1), another mitotic kinase implicated in cell polarity. They find that although PLK-1 suppresses the formation of ectopic polarized domains during meiosis I, unlike AIR-1, PLK-1 is dispensable for symmetry breaking. Overall, the findings suggest temporally distinct roles of AIR-1 in coordinating PAR protein localization during development.
