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: Integration of collective cell direction and coordination is believed to ensure collective guidance for efficient movement. Previous studies demonstrated that chemokine receptors PVR and EGFR govern a gradient of Rac1 activity essential for collective guidance of Drosophila border cells, whose mechanistic insight is unknown. By monitoring and manipulating subcellular Rac1 activity, here we reveal two switchable Rac1 pools at border cell protrusions and supracellular cables, two important structures responsible for direction and coordination. Rac1 and Rho1 form a positive feedback loop that guides mechanical coupling at cables to achieve migration coordination. Rac1 cooperates with Cdc42 to control protrusion growth for migration direction, as well as to regulate the protrusion-cable exchange, linking direction and coordination. PVR and EGFR guide correct Rac1 activity distribution at protrusions and cables. Therefore, our studies emphasize the existence of a balance between two Rac1 pools, rather than a Rac1 activity gradient, as an integrator for the direction and coordination of collective cell migration.

Abstract: Pulsatile actomyosin contractility, important in tissue morphogenesis, has been studied mainly in apical but less in basal domains. Basal myosin oscillation underlying egg chamber elongation is regulated by both cell-matrix and cell-cell adhesions. However, the mechanism by which these two adhesions govern basal myosin oscillation and tissue elongation is unknown. Here we demonstrate that cell-matrix adhesion positively regulates basal junctional Rho1 activity and medio-basal ROCK and myosin activities, thus strongly controlling tissue elongation. Differently, cell-cell adhesion governs basal myosin oscillation through controlling medio-basal distributions of both ROCK and myosin signals, which are related to the spatial limitations of cell-matrix adhesion and stress fibres. Contrary to cell-matrix adhesion, cell-cell adhesion weakly affects tissue elongation. In vivo optogenetic protein inhibition spatiotemporally confirms the different effects of these two adhesions on basal myosin oscillation. This study highlights the activity and distribution controls of basal myosin contractility mediated by cell-matrix and cell-cell adhesions, respectively, during tissue morphogenesis.