As they enter mitosis, animal cells undergo profound actin-dependent changes in shape to become round. Here we identify the Cdk1 substrate, Ect2, as a central regulator of mitotic rounding, thus uncovering a link between the cell-cycle machinery that drives mitotic entry and its accompanying actin remodeling. Ect2 is a RhoGEF that plays a well-established role in formation of the actomyosin contractile ring at mitotic exit, through the local activation of RhoA. We find that Ect2 first becomes active in prophase, when it is exported from the nucleus into the cytoplasm, activating RhoA to induce the formation of a mechanically stiff and rounded metaphase cortex. Then, at anaphase, binding to RacGAP1 at the spindle midzone repositions Ect2 to induce local actomyosin ring formation. Ect2 localization therefore defines the stage-specific changes in actin cortex organization critical for accurate cell division.
► Ect2 drives dynamic changes in cell shape throughout mitosis ► Ect2 induces actin-dependent changes in cortical mechanics at mitotic onset ► Ect2's distinct functions are achieved through changes in subcellular localization ► Actin remodeling for animal cell division begins at mitotic entry
Cell division is accompanied by dramatic changes in cell shape, which Matthews et al. show are regulated by the Cdk1 substrate Ect2. At mitotic onset, Ect2 leaves the nucleus to activate RhoA and cortical actomyosin, driving mitotic rounding. It is then repositioned at mitotic exit to drive actomyosin ring formation.