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Abstract

Asymmetric cell division plays a pivotal role in orchestrating cell type diversification during metazoan development by generating two daughter cells with distinct fates, shapes, and sizes. In Caenorhabditis elegans, the evolutionarily conserved Wnt signaling pathway controls asymmetric cell division. While previous studies have revealed the requirement of asymmetric localization of Wnt signaling pathway components in asymmetric division, the precise mechanism governing this process remains unclear. This thesis aims to dissect the role of cortical actomyosin during the asymmetric cell division of the endomesodermal precursor, the EMS cell. Utilizing a spinning disk confocal microscope, I quantitatively analyzed cortical actomyosin dynamics through the visualization of non-muscle myosin II and F-actin. I found that cortical flow, F-actin orientation, and F-actin abundance are asymmetrically regulated during cytokinesis in a Wnt-dependent manner. Live-imaging suggests that asymmetric cortical flow generates F-actin abundance asymmetry through the loss of F-actin from the posterior cell cortex. Asymmetric F-actin abundance is proposed as a cause of the cell size asymmetry in other systems. Consistently, we found that both Wnt and F-actin are required for the cell size asymmetry after EMS cell division. Together, this study suggests that Wnt-dependent regulation of cortical flow generates asymmetric F-actin abundance, thereby controlling the cell size asymmetry during EMS cell division. The obtained knowledge should shed light on the mechanism underlying asymmetric partitioning of dividing cells in other cell types or different organisms.