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The Johns Hopkins University, 현 고려대학교

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Sci Rep, Published 03 August 2012 | https://doi.org/10.1038/srep00555 Actin cap associated focal adhesions and their distinct role in cellular mechanosensing

Dong-Hwee Kim1,2, Shyam B. Khatau1,2, Yunfeng Feng1,3, Sam Walcott1,4*, Sean X. Sun1,2,4, Gregory D. Longmore1,3 & Denis Wirtz1,2

1Johns Hopkins Physical Sciences in Oncology Center, The Johns Hopkins University, Baltimore, Maryland 21218, USA,
2Department of Chemical and Biomolecular Engineering, The Johns Hopkins University, Baltimore, Maryland 21218, USA,
3Departments of Medicine and Cell Biology and Physiology, Washington University School of Medicine, St. Louis, MO 63110, USA,
4Department of Mechanical Engineering, The Johns Hopkins University, Baltimore, Maryland 21218, USA.

Correspondence and requests for materials should be addressed to D.W. or G.D.L.

Abstract

The ability for cells to sense and adapt to different physical microenvironments plays a critical role in development, immune responses and cancer metastasis. Here we identify a small subset of focal adhesions that terminate fibers in the actin cap, a highly ordered filamentous actin structure that is anchored to the top of the nucleus by the LINC complexes; these differ from conventional focal adhesions in morphology, subcellular organization, movements, turnover dynamics and response to biochemical stimuli. Actin cap associated focal adhesions (ACAFAs) dominate cell mechanosensing over a wide range of matrix stiffness, an ACAFA-specific function regulated by actomyosin contractility in the actin cap, while conventional focal adhesions are restrictively involved in mechanosensing for extremely soft substrates. These results establish the perinuclear actin cap and associated ACAFAs as major mediators of cellular mechanosensing and a critical element of the physical pathway that transduce mechanical cues all the way to the nucleus.

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