Contractile forces regulate cell division in three-dimensional environments
Abstract
Physical forces direct the orientation of the cell division axis for cells cultured on rigid, two-dimensional (2D) substrates. The extent to which physical forces regulate cell division in three-dimensional (3D) environments is not known. Here, we combine live-cell imaging with digital volume correlation to map 3D matrix displacements and identify sites at which cells apply contractile force to the matrix as they divide. Dividing cells embedded in fibrous matrices remained anchored to the matrix by long, thin protrusions. During cell rounding, the cells released adhesive contacts near the cell body while applying tensile forces at the tips of the protrusions to direct the orientation of the cell division axis. After cytokinesis, the daughter cells respread into matrix voids and invaded the matrix while maintaining traction forces at the tips of persistent and newly formed protrusions. Mechanical interactions between cells and the extracellular matrix constitute an important mechanism for regulation of cell division in 3D environments.
Additional Information
© 2014 Lesman et al. This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.rupress.org/terms). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 3.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/3.0/). Submitted: 6 September 2013 Accepted: 25 March 2014. We thank Scott Fraser for providing the transfected fibroblasts. We thank the Biological Imaging Center at Caltech for use of the two-photon microscope. This research was supported by grants from the National Science Foundation (Division of Materials Research No. 0520565 and 1206121). J. Notbohm was supported by the Department of Defense through the National Defense Science and Engineering Graduate Fellowship Program. A. Lesman was supported in part by the Rothschild fellowship foundation. The authors declare no competing financial interests.Attached Files
Published - J_Cell_Biol-2014-Lesman-155-62.pdf
Supplemental Material - JCB_201309029_V1.mp4
Supplemental Material - JCB_201309029_V10.mp4
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Additional details
- PMCID
- PMC4003238
- Eprint ID
- 46067
- Resolver ID
- CaltechAUTHORS:20140604-075231845
- DMR-0520565
- NSF
- DMR-1206121
- NSF
- National Defense Science and Engineering Graduate (NDSEG) Fellowship
- Rothschild Foundation
- Created
-
2014-06-04Created from EPrint's datestamp field
- Updated
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2021-11-10Created from EPrint's last_modified field
- Caltech groups
- GALCIT