Published in

National Academy of Sciences, Proceedings of the National Academy of Sciences, 52(117), p. 33263-33271, 2020

DOI: 10.1073/pnas.2010960117

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Actin-ring segment switching drives nonadhesive gap closure

This paper is made freely available by the publisher.
This paper is made freely available by the publisher.

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Abstract

Significance Gap closure to eliminate physical discontinuities and restore tissue integrity is a fundamental process in normal development and repair of damaged tissues and organs. Here, we report a previously unexplored gap-closure mechanism by which cell proliferation, collective cell migration, large-scale intercellular actin-network remodeling, and purse-string contraction act in a highly coordinated manner to restore the gap. In distinct contrast to the classical purse-string contraction mechanism, this mechanism involves intercellular switching of actin-cable segments at the gap front, which effectively empowers the actin cable for gap closure. Our study highlights the principles of wound healing driven by the close reciprocity between mechanics and cellular remodeling and might inspire mechanobiological intervention strategies for embryogenesis, tissue repair, antimetastasis, and plastic surgery.