Loss of G[subscript α12/13] exacerbates apical area-dependence of actomyosin contractility
Name
Xie-2016-Loss of Galpha12_13.pdf
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4.65 MB
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Author(s)
Xie, Shicong
Mason, Frank M
Martin, Adam C
Alternative Title
Loss of Gα12/13 exacerbates apical area dependence of actomyosin contractility
Date Issued
August 2016
Journal
Molecular Biology of the Cell
Publisher
American Society for Cell Biology
Citation
Xie, S., F. M. Mason, and A. C. Martin. “Loss of G 12/13 Exacerbates Apical Area-Dependence of Actomyosin Contractility.” Molecular Biology of the Cell (2016): n. pag. © 2016 American Society for Cell Biology
Version
Final published version
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.
MIT Department
Massachusetts Institute of Technology. Computational and Systems Biology Program
Massachusetts Institute of Technology. Department of Biology
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Creative Commons Attribution-NonCommercial-ShareAlike 3.0
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DOI of Published Version
https://doi.org/10.1091/mbc.E16-05-0305
