Cortical F-actin filament organization corrals E-cadherin/HMR-1 during cytokinetic furrow ingression in C. elegans embryos

In metazoan cells, the delicate equilibrium between proliferative cell division and inter-cellular adhesion is crucial for achieving growth while maintaining tissue integrity and homeostasis. The transmembrane adhesion receptor, E-cadherin, not only facilitates cell-cell adhesion but modulates cytokinesis by impeding cortical F-actin flow and inhibiting actomyosin contractility. In the C. elegans zygote, newly established cell-cell interfaces following cytokinesis lack E-cadherin/HMR-1 (Padmanabhan et al., 2017b). The mechanisms responsible for the spatial exclusion of HMR-1, however remain elusive. Here, we show that HMR-1 is actively prevented from entering the cytokinetic furrow zone during early embryonic divisions in C. elegans. The compact alignment of unbranched F-actin filaments polymerized by the formin/CYK-1 restricts HMR-1 from entering the ingressing furrow. This corralling phenomenon depends on the physical association between HMR-1 and F-actin mediated via the {beta}- and - catenins, HMP-2 and HMP-1, respectively. Our findings reveal a previously unknown reciprocal regulatory relationship between cell adhesion and cell division machineries, ensuring the precise orchestration of the cytokinesis during embryonic development.