Integration of contractile forces during tissue invagination
Name
Martin JCB.pdf
Description
main article
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3.68 MB
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Author(s)
Martin, Adam C.
Gelbart, Michael A.
Fernandez-Gonzalez, Rodrigo
Kaschube, Matthias
Wieschaus, Eric F.
Date Issued
March 2010
Journal
Journal of Cell Biology
Publisher
Rockefeller University Press
Citation
Martin, A. C. et al. “Integration of contractile forces during tissue invagination.” The Journal of Cell Biology 188 (2010): 735-749.
Version
Author's final manuscript
Abstract
Contractile forces generated by the actomyosin cytoskeleton within individual cells collectively generate tissue-level force during epithelial morphogenesis. During Drosophila mesoderm invagination, pulsed actomyosin meshwork contractions and a ratchet-like stabilization of cell shape drive apical constriction. Here, we investigate how contractile forces are integrated across the tissue. Reducing adherens junction (AJ) levels or ablating actomyosin meshworks causes tissue-wide epithelial tears, which release tension that is predominantly oriented along the anterior–posterior (a-p) embryonic axis. Epithelial tears allow cells normally elongated along the a-p axis to constrict isotropically, which suggests that apical constriction generates anisotropic epithelial tension that feeds back to control cell shape. Epithelial tension requires the transcription factor Twist, which stabilizes apical myosin II, promoting the formation of a supracellular actomyosin meshwork in which radial actomyosin fibers are joined end-to-end at spot AJs. Thus, pulsed actomyosin contractions require a supracellular, tensile meshwork to transmit cellular forces to the tissue level during morphogenesis.
MIT Department
Massachusetts Institute of Technology. Department of Biology
Terms of Use
Creative Commons Attribution-Noncommercial-Share Alike 3.0
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DOI of Published Version
https://doi.org/10.1083/jcb.200910099
