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A three-component mechanism for fibroblast migration with a contractile cell body that couples a myosin II–independent propulsive anterior to a myosin II–dependent resistive tail
To understand the mechanism of cell migration, we cultured fibroblasts on micropatterned tracks to induce persistent migration with a highly elongated morphology and well-defined polarity, which allows microfluidic pharmacological manipulations of regional functions. The function of myosin II was pr...
Autores principales: | , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
The American Society for Cell Biology
2012
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3338433/ https://www.ncbi.nlm.nih.gov/pubmed/22398722 http://dx.doi.org/10.1091/mbc.E11-06-0556 |
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author | Guo, Wei-hui Wang, Yu-li |
author_facet | Guo, Wei-hui Wang, Yu-li |
author_sort | Guo, Wei-hui |
collection | PubMed |
description | To understand the mechanism of cell migration, we cultured fibroblasts on micropatterned tracks to induce persistent migration with a highly elongated morphology and well-defined polarity, which allows microfluidic pharmacological manipulations of regional functions. The function of myosin II was probed by applying inhibitors either globally or locally. Of interest, although global inhibition of myosin II inhibited tail retraction and caused dramatic elongation of the posterior region, localized inhibition of the cell body inhibited nuclear translocation and caused elongation of the anterior region. In addition, local application of cytochalasin D at the tip inhibited frontal extension without inhibiting forward movement of the cell nucleus, whereas local treatment posterior to the nucleus caused reversal of nuclear movement. Imaging of cortical dynamics indicated that the region around the nucleus is a distinct compression zone where activities of anterior and posterior regions converge. These observations suggest a three-component model of cell migration in which a contractile middle section is responsible for the movement of a bulky cell body and the detachment/retraction of a resistive tail, thereby allowing these regions to undergo coordinated movement with a moving anterior region that carries little load. |
format | Online Article Text |
id | pubmed-3338433 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2012 |
publisher | The American Society for Cell Biology |
record_format | MEDLINE/PubMed |
spelling | pubmed-33384332012-07-16 A three-component mechanism for fibroblast migration with a contractile cell body that couples a myosin II–independent propulsive anterior to a myosin II–dependent resistive tail Guo, Wei-hui Wang, Yu-li Mol Biol Cell Articles To understand the mechanism of cell migration, we cultured fibroblasts on micropatterned tracks to induce persistent migration with a highly elongated morphology and well-defined polarity, which allows microfluidic pharmacological manipulations of regional functions. The function of myosin II was probed by applying inhibitors either globally or locally. Of interest, although global inhibition of myosin II inhibited tail retraction and caused dramatic elongation of the posterior region, localized inhibition of the cell body inhibited nuclear translocation and caused elongation of the anterior region. In addition, local application of cytochalasin D at the tip inhibited frontal extension without inhibiting forward movement of the cell nucleus, whereas local treatment posterior to the nucleus caused reversal of nuclear movement. Imaging of cortical dynamics indicated that the region around the nucleus is a distinct compression zone where activities of anterior and posterior regions converge. These observations suggest a three-component model of cell migration in which a contractile middle section is responsible for the movement of a bulky cell body and the detachment/retraction of a resistive tail, thereby allowing these regions to undergo coordinated movement with a moving anterior region that carries little load. The American Society for Cell Biology 2012-05-01 /pmc/articles/PMC3338433/ /pubmed/22398722 http://dx.doi.org/10.1091/mbc.E11-06-0556 Text en © 2012 Guo and Wang. This article is distributed by The American Society for Cell Biology under license from the author(s). Two months after publication it is available to the public under an Attribution–Noncommercial–Share Alike 3.0 Unported Creative Commons License (http://creativecommons.org/licenses/by-nc-sa/3.0). “ASCB®,” “The American Society for Cell Biology®,” and “Molecular Biology of the Cell®” are registered trademarks of The American Society of Cell Biology. |
spellingShingle | Articles Guo, Wei-hui Wang, Yu-li A three-component mechanism for fibroblast migration with a contractile cell body that couples a myosin II–independent propulsive anterior to a myosin II–dependent resistive tail |
title | A three-component mechanism for fibroblast migration with a contractile cell body that couples a myosin II–independent propulsive anterior to a myosin II–dependent resistive tail |
title_full | A three-component mechanism for fibroblast migration with a contractile cell body that couples a myosin II–independent propulsive anterior to a myosin II–dependent resistive tail |
title_fullStr | A three-component mechanism for fibroblast migration with a contractile cell body that couples a myosin II–independent propulsive anterior to a myosin II–dependent resistive tail |
title_full_unstemmed | A three-component mechanism for fibroblast migration with a contractile cell body that couples a myosin II–independent propulsive anterior to a myosin II–dependent resistive tail |
title_short | A three-component mechanism for fibroblast migration with a contractile cell body that couples a myosin II–independent propulsive anterior to a myosin II–dependent resistive tail |
title_sort | three-component mechanism for fibroblast migration with a contractile cell body that couples a myosin ii–independent propulsive anterior to a myosin ii–dependent resistive tail |
topic | Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3338433/ https://www.ncbi.nlm.nih.gov/pubmed/22398722 http://dx.doi.org/10.1091/mbc.E11-06-0556 |
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