Persistent cell contacts enable E-cadherin/HMR-1- and PAR-3-based symmetry breaking within a developing C. elegans epithelium

Publication Date

10-9-2023

Document Type

Article

Publication Title

Developmental Cell

Volume

58

Issue

19

DOI

10.1016/j.devcel.2023.07.008

First Page

1830

Last Page

1846.e12

Abstract

Tissue-wide patterning is essential to multicellular development, requiring cells to individually generate polarity axes and coordinate them in space and time with neighbors. Using the C. elegans intestinal epithelium, we identified a patterning mechanism that is informed by cell contact lifetime asymmetry and executed via the scaffolding protein PAR-3 and the transmembrane protein E-cadherin/HMR-1. Intestinal cells break symmetry as PAR-3 and HMR-1 recruit apical determinants into punctate “local polarity complexes” (LPCs) at homotypic contacts. LPCs undergo an HMR-1-based migration to a common midline, thereby establishing tissue-wide polarity. Thus, symmetry breaking results from PAR-3-dependent intracellular polarization coupled to HMR-1-based tissue-level communication, which occurs through a non-adhesive signaling role for HMR-1. Differential lifetimes between homotypic and heterotypic cell contacts are created by neighbor exchanges and oriented divisions, patterning where LPCs perdure and thereby breaking symmetry. These cues offer a logical and likely conserved framework for how epithelia without obvious molecular asymmetries can polarize.

Funding Number

P40 OD010440

Funding Sponsor

National Institutes of Health

Keywords

C. elegans, cell contact, E-cadherin, epithelia, HMR-1, morphogenesis, PAR-3, polarity, symmetry breaking

Department

Biological Sciences

Link to Full Text

Share

COinS