Pulsed contractility is a dynamic form of actomyosin contractility that underlies many different kinds of morphogenetic processes. In a new paper published in the Journal of Cell Biology, CMB graduate student John Michaux and colleagues in the Munro Lab combine multicolor live imaging, single molecule analysis, genetic manipulations and mathematical modeling to identify a core biochemical circuit for pulsed contractility in early C. elegans embryos. They show that pulsed contractions are generated by intrinsically excitable RhoA dynamics, involving fast autoactivation of RhoA and delayed negative feedback through local actin-dependent recruitment of the RhoGAPs RGA-3/4.