Journal
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
Volume 111, Issue 41, Pages 14770-14775Publisher
NATL ACAD SCIENCES
DOI: 10.1073/pnas.1414498111
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Funding
- National Institutes of Health [P01 GM078586, R01 GM096188]
- National Science Foundation [DMS 1309542, DMS 1319731]
- Center for Theoretical Biological Physics Grant [PHY-0822283]
- Direct For Mathematical & Physical Scien
- Division Of Mathematical Sciences [1319731] Funding Source: National Science Foundation
- Division Of Physics
- Direct For Mathematical & Physical Scien [1427654, 1308264] Funding Source: National Science Foundation
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Pairs of endothelial cells on adhesive micropatterns rotate persistently, but pairs of fibroblasts do not; coherent rotation is present in normal mammary acini and kidney cells but absent in cancerous cells. Why? To answer this question, we develop a computational model of pairs of mammalian cells on adhesive micropatterns using a phase field method and study the conditions under which persistent rotational motion (PRM) emerges. Our model couples the shape of the cell, the cell's internal chemical polarity, and interactions between cells such as volume exclusion and adhesion. We show that PRM can emerge from this minimal model and that the cell-cell interface may be influenced by the nucleus. We study the effect of various cell polarity mechanisms on rotational motion, including contact inhibition of locomotion, neighbor alignment, and velocity alignment, where cells align their polarity to their velocity. These polarity mechanisms strongly regulate PRM: Small differences in polarity mechanisms can create significant differences in collective rotation. We argue that the existence or absence of rotation under confinement may lead to insight into the cell's methods for coordinating collective cell motility.
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