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Myosin IIA deficient cells migrate efficiently despite reduced traction forces at cell periphery
Cell motility is a cornerstone of embryogenesis, tissue remodeling and repair, and cancer cell invasion. It is generally thought that migrating cells grab and exert traction force onto the extracellular matrix in order to pull the cell body forward. While previous studies have shown that myosin II d...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
The Company of Biologists
2013
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3625864/ https://www.ncbi.nlm.nih.gov/pubmed/23616920 http://dx.doi.org/10.1242/bio.20133707 |
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author | Jorrisch, Melissa H. Shih, Wenting Yamada, Soichiro |
author_facet | Jorrisch, Melissa H. Shih, Wenting Yamada, Soichiro |
author_sort | Jorrisch, Melissa H. |
collection | PubMed |
description | Cell motility is a cornerstone of embryogenesis, tissue remodeling and repair, and cancer cell invasion. It is generally thought that migrating cells grab and exert traction force onto the extracellular matrix in order to pull the cell body forward. While previous studies have shown that myosin II deficient cells migrate efficiently, whether these cells exert traction forces during cell migration in the absence of the major contractile machinery is currently unknown. Using an array of micron-sized pillars as a force sensor and shRNA specific to each myosin II isoform (A and B), we analyzed how myosin IIA and IIB individually regulate cell migration and traction force generation. Myosin IIA and IIB localized preferentially to the leading edge where traction force was greatest, and the trailing edge, respectively. When individual myosin II isoforms were depleted by shRNA, myosin IIA deficient cells lost actin stress fibers and focal adhesions, whereas myosin IIB deficient cells maintained similar actin organization and focal adhesions as wild-type cells. Interestingly, myosin IIA deficient cells migrated faster than wild-type or myosin IIB deficient cells on both a rigid surface and a pillar array, yet myosin IIA deficient cells exerted significantly less traction force at the leading edge than wild-type or myosin IIB deficient cells. These results suggest that, in the absence of myosin IIA mediated force-generating machinery, cells move with minimal traction forces at the cell periphery, thus demonstrating the remarkable ability of cells to adapt and migrate. |
format | Online Article Text |
id | pubmed-3625864 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2013 |
publisher | The Company of Biologists |
record_format | MEDLINE/PubMed |
spelling | pubmed-36258642013-04-24 Myosin IIA deficient cells migrate efficiently despite reduced traction forces at cell periphery Jorrisch, Melissa H. Shih, Wenting Yamada, Soichiro Biol Open Research Article Cell motility is a cornerstone of embryogenesis, tissue remodeling and repair, and cancer cell invasion. It is generally thought that migrating cells grab and exert traction force onto the extracellular matrix in order to pull the cell body forward. While previous studies have shown that myosin II deficient cells migrate efficiently, whether these cells exert traction forces during cell migration in the absence of the major contractile machinery is currently unknown. Using an array of micron-sized pillars as a force sensor and shRNA specific to each myosin II isoform (A and B), we analyzed how myosin IIA and IIB individually regulate cell migration and traction force generation. Myosin IIA and IIB localized preferentially to the leading edge where traction force was greatest, and the trailing edge, respectively. When individual myosin II isoforms were depleted by shRNA, myosin IIA deficient cells lost actin stress fibers and focal adhesions, whereas myosin IIB deficient cells maintained similar actin organization and focal adhesions as wild-type cells. Interestingly, myosin IIA deficient cells migrated faster than wild-type or myosin IIB deficient cells on both a rigid surface and a pillar array, yet myosin IIA deficient cells exerted significantly less traction force at the leading edge than wild-type or myosin IIB deficient cells. These results suggest that, in the absence of myosin IIA mediated force-generating machinery, cells move with minimal traction forces at the cell periphery, thus demonstrating the remarkable ability of cells to adapt and migrate. The Company of Biologists 2013-02-06 /pmc/articles/PMC3625864/ /pubmed/23616920 http://dx.doi.org/10.1242/bio.20133707 Text en © 2013. Published by The Company of Biologists Ltd http://creativecommons.org/licenses/by-nc-sa/3.0 This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial Share Alike License (http://creativecommons.org/licenses/by-nc-sa/3.0/). |
spellingShingle | Research Article Jorrisch, Melissa H. Shih, Wenting Yamada, Soichiro Myosin IIA deficient cells migrate efficiently despite reduced traction forces at cell periphery |
title | Myosin IIA deficient cells migrate efficiently despite reduced traction forces at cell periphery |
title_full | Myosin IIA deficient cells migrate efficiently despite reduced traction forces at cell periphery |
title_fullStr | Myosin IIA deficient cells migrate efficiently despite reduced traction forces at cell periphery |
title_full_unstemmed | Myosin IIA deficient cells migrate efficiently despite reduced traction forces at cell periphery |
title_short | Myosin IIA deficient cells migrate efficiently despite reduced traction forces at cell periphery |
title_sort | myosin iia deficient cells migrate efficiently despite reduced traction forces at cell periphery |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3625864/ https://www.ncbi.nlm.nih.gov/pubmed/23616920 http://dx.doi.org/10.1242/bio.20133707 |
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