LAUSR

morphogenesis coupled to cell proliferation. Coordination of cell shape changes and cell divisions requires spatially-biased remodelling of actomyosin cytoskeleton in response to intrinsic or extrinsic inputs. In Caenorhabditis elegans zygotes, transient flows of cortical actomyosin instruct the asymmetry of the first mitotic division. However, the mitotic signal that patterns excitation and repression of contractile actomyosin remains poorly understood. We present evidence that the mitotic kinase Aurora-A dictates local and global remodelling of cortical actomyosin to facilitate asymmetric cell division. Aurora-A accumulates at mitotic centrosomes to locally disassemble cortical myosin at the proximal cortex, leading to a gradient in actomyosin contractility that drive cortical flows. We demonstrate that induction of cortical flows is independent of a role of Aurora-A in centrosome maturation. In contrast, Aurora-A in cytoplasm stimulates global disassembly of cortical myosin during late prophase. Loss of Aurora-A caused sustained activation of RhoA GTPase throughout the cortex during prophase, suggesting Aurora-A as a local and global inhibitor of RhoA. We thus propose a mechanism by which cell cycle progression is coordinated with actomyosin remodelling through mitotic kinase Aurora-A. To identify the downstream targets of Aurora-A, we performed in vivo large-scale protein interaction studies complemented with in vitro kinase assay screen. We will present our current progress and discuss how Aurora-A controls two distinct phases of myosin remodelling for asymmetric cell division.