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

## TL;DR

This study shows how actin filaments prevent E-cadherin from entering the cell division zone, ensuring accurate cell division during embryonic development.

## Contribution

The paper reveals a novel mechanism where actin filaments physically exclude E-cadherin from the division furrow to ensure cytokinesis fidelity.

## Key findings

- CYK-1/formin-polymerized actin filaments restrict HMR-1/E-cadherin mobility into the cytokinetic furrow.
- Disrupting cortical actin leads to HMR-1 accumulation in the furrow and increased cytokinesis failure.
- Co-depletion of HMR-1 rescues cytokinesis failure caused by actin disruption.

## Abstract

Localization of the cell adhesion receptor E-cadherin within the furrow is associated with reduced cytokinetic fidelity. Cortical organization of formin-polymerized linear actin filaments at the division zone physically associates with E-cadherin and restricts its lateral mobility into the cytokinetic furrow.

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 Caenorhabditis elegans 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.