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Abstract

Contraction of cortical actomyosin networks drives cell shape changes and is of fundamental importance during morphogenesis of multicellular organisms. Over the course of the last decade, an increasing number of studies has demonstrated the key role played by localized myosin activation at the apical surface of epithelial cells during a wide range of tissue morphogenetic processes. However, recent in vitro studies and computational models suggest that the architecture of the underlying actin network is also important. Furthermore, whether apical myosin-derived forces alone are sufficient to drive cell shape changes and morphogenesis remains highly debated, as the role of the basolateral surface must also be taken into account. In this thesis, by focusing on the dynamic remodeling of a basally localized actomyosin network required for early Drosophila embryonic development, I provide strong evidence in support of the role of actin network organization in controlling contractility. Using a combination of genetic, biochemical, and optogenetic approaches, I identified a mechanism based on actin crosslinkers, which regulate the spatial organization of actin networks and thereby time actomyosin contraction during cellularization, the transformation of the syncytial embryo in 6000 mononucleated epithelial cells. I further demonstrate that following cellularization, myosin-II activity at the basal surface of ventral cells must be downregulated in order to allow efficient apical constriction, cell wedging and ventral furrow invagination. Collectively the results presented in this thesis provide novel insights into the underlying spatiotemporal organization of actomyosin networks and molecular principles regulating actomyosin contraction during tissue morphogenesis.