Curated Optogenetic Publication Database

Abstract: Pulsatile actomyosin networks emerge as a widespread mechanism driving tissue morphogenesis. Compared with myosin-II pulses, F-actin pulses are largely unexplored. By studying Drosophila oogenesis, we report that basal pulsatile actomyosin networks consist of F-actin bundle and meshwork architectures, implicating the existence of different F-actin microstructures and corresponding nucleators. Here, Rac1 and the Scar/WAVE-Arp2/3 complex (branched F-actin nucleator), exhibiting constant levels, are necessary to support F-actin pulsation, whereas pulses of Dia (unbranched F-actin nucleator) trigger F-actin pulsation. The pulsatile F-actin networks recruit the F-actin turnover regulator cofilin, thus generating cofilin pulses. Cofilin at relatively low concentration can cooperate with F-actin nucleators to amplify F-actin and enhance its pulsation, while cofilin at relatively high concentration might trigger the F-actin disassembly to attenuate its pulsation. These two different effects of cofilin on F-actin pulsation were confirmed by Zdk-cofilin optogenetics. Rac1 signaling, Dia, and cofilin are also crucial for F-actin pulses in border cell migration. Our findings thus reveal a coordinated regulation of F-actin pulses conferring actomyosin contractility in morphogenesis and cell migration.

Abstract: The actomyosin cytoskeleton, a key stress-producing unit in epithelial cells, oscillates spontaneously in a wide variety of systems. Although much of the signal cascade regulating myosin activity has been characterized, the origin of such oscillatory behavior is still unclear. Here, we show that basal myosin II oscillation in Drosophila ovarian epithelium is not controlled by actomyosin cortical tension, but instead relies on a biochemical oscillator involving ROCK and myosin phosphatase. Key to this oscillation is a diffusive ROCK flow, linking junctional Rho1 to medial actomyosin cortex, and dynamically maintained by a self-activation loop reliant on ROCK kinase activity. In response to the resulting myosin II recruitment, myosin phosphatase is locally enriched and shuts off ROCK and myosin II signals. Coupling Drosophila genetics, live imaging, modeling, and optogenetics, we uncover an intrinsic biochemical oscillator at the core of myosin II regulatory network, shedding light on the spatio-temporal dynamics of force generation.