# Actomyosin contractility drives apical polarization and membrane transport during tubulogenesis

## TL;DR

This study shows how actomyosin contractility helps cells form lumens during tubulogenesis by coordinating membrane transport and polarization.

## Contribution

The paper reveals a novel mechanism of actomyosin-driven transport and lumen growth involving ERM proteins and ECM interactions.

## Key findings

- Actomyosin contractility positions apical lumens by centralizing apical determinants on cell contacts.
- ERM proteins and ECM are essential for basal membrane internalization and lumen growth.
- Cortical and cytoplasmic transport modes are integrated to enable rapid lumen formation.

## Abstract

Lumen formation during tubulogenesis requires the large-scale redistribution of cellular material, but the in vivo mechanisms remain unclear. Using the ascidian notochord as a tractable model, we show that actomyosin contractility orchestrates sequential, spatially distinct modes of cortical and cytoplasmic transport to promote lumen initiation and growth: lateral actomyosin centralizes apical determinants on cell contacts to position apical lumens; cyclic detachment and inward contraction of actomyosin bundles from a basal equatorial contractile ring drives internalization and transport of basal membranes toward the apical lumen surface to enable lumen growth. Basal membrane internalization/transport and lumen growth require both Ezrin/Radixin/Moesin (ERM) proteins and extracellular matrix (ECM). ERM promotes equatorial contractility and transmits inward contractile forces to basal membranes, while broad attachment to ECM resists inward forces to promote equatorial detachment. These findings reveal how cells integrate cortical and cytoplasmic modes of transport, driven by actomyosin contractility, to enable rapid lumen formation and likely other types of cellular remodeling.