At the end of cell division, in a process called cytokinesis, the content of mother cell is segregated to the two daughter cells. During cytokinesis a contractile actin-myosin ring assembles underneath the plasma membrane at the cell equator. Contractile ring formation has to be coupled temporally to cell cycle progression and spatially to chromosome segregation. Failure in cytokinesis results in tetraploid cells, which have increased genomic instability and a tendency for oncogenic transformation. Contractile ring formation is controlled by the mitotic spindle and thereby chromosome segregation is coordinated with contractile ring formation. The mitotic spindle promotes the activation of the GTPase RhoA in a narrow region at the cell equator. RhoA controls contractile ring formation by activating myosin II and inducing the formation of filamentous actin network. How the mitotic spindle controls RhoA activation during anaphase and how active RhoA is restricted to a narrow region at the cell equator is currently unknown. In the lab we use a combination of biochemistry, genetics and quantitative live-cell microscopy in the C. elegans one-cell embryo and human tissue culture cells to address these questions.