Dissemin is shutting down on January 1st, 2025

Published in

American Society for Cell Biology, Molecular Biology of the Cell, 22(27), p. 3526-3536

DOI: 10.1091/mbc.e16-05-0305

Links

Tools

Export citation

Search in Google Scholar

Loss of Gα12/13 exacerbates apical area dependence of actomyosin contractility

Journal article published in 2016 by Shicong Xie, Frank M. Mason ORCID, Adam C. Martin
This paper is made freely available by the publisher.
This paper is made freely available by the publisher.

Full text: Download

Red circle
Preprint: archiving forbidden
Green circle
Postprint: archiving allowed
Orange circle
Published version: archiving restricted
Data provided by SHERPA/RoMEO

Abstract

During development, coordinated cell shape changes alter tissue shape. In the Drosophila ventral furrow and other epithelia, apical constriction of hundreds of epithelial cells folds the tissue. Genes in the G[subscript α12/13] pathway coordinate collective apical constriction, but the mechanism of coordination is poorly understood. Coupling live-cell imaging with a computational approach to identify contractile events, we discovered that differences in constriction behavior are biased by initial cell shape. Disrupting G[subscript α12/13] exacerbates this relationship. Larger apical area is associated with delayed initiation of contractile pulses, lower apical E-cadherin and F-actin levels, and aberrantly mobile Rho-Kinase structures. Our results suggest that loss of G[subscript α12/13] disrupts apical actin cortex organization and pulse initiation in a size-dependent manner. We propose that G[subscript α12/13] robustly organizes the apical cortex despite variation in apical area to ensure the timely initiation of contractile pulses in a tissue with heterogeneity in starting cell shape.