Embryonic cells harness actomyosin contractility to move, change shape and to produce long-range flows that redistribute their internal components. We are interested in the basic principles that underlie dynamic control of cortical actomyosin contractility. How do contractility and cortical flow emerge from microscopic interactions among actin filaments, crosslinking proteins, and myosin motors? How do embryonic cells tune contractility through local modulation of filament assembly, disassembly and motor activity? How do they integrate biochemical signaling and contractility to pattern force generation in space and time? We currently focus in three areas: (a) Self-organization of the contractile ring during cytokinesis, (b) Spatiotemporal control of pulsed actomyosin contractility through dynamic coupling of RhoA signaling and actomyosin dynamics. (c) Dynamic coupling of actomyosin contractility and Par protein dynamics during polarization.