F-actin organization excludes E-cadherin from the division furrow to ensure cytokinesis fidelity

Maintaining intercellular adhesion during proliferative cell division is essential for ensuring tissue integrity during embryonic development. How these two processes are coordinated in vivo remains poorly understood. During early <i>Caenorhabditis elegans</i> embryonic divisions, the cell adhesion receptor, HMR-1/E-cadherin, is absent from the cytokinetic furrow zone and the newly established cell-cell interface. We investigated mechanisms underlying this spatial exclusion of HMR-1 from the furrow zone. We find that crosslinking and compact alignment of CYK-1/formin-polymerized unbranched actin filaments in the cytokinetic furrow restrict the mobility of HMR-1 into the division zone. Disruption of cortical actin organization through depletion of CYK-1 or myosin/NMY-2 leads to HMR-1 accumulation in the furrow zone, and a concomitant increase in cytokinesis failure. Notably, co-depleting HMR-1 in these embryos rescues the observed cytokinesis failure phenotype. Our findings reveal a reciprocal regulatory relationship between cell adhesion and cell division machinery, essential for precise and timely completion of cytokinesis during embryonic development.