Structural links from the nucleus to the cytoskeleton and to the extracellular environment play a role in direct mechanosensing by nuclear factors. Here, we highlight recent studies that illustrate nuclear mechanosensation processes ranging from DNA repair and nuclear protein phospho-modulation to chromatin reorganization, lipase activation by dilation, and reversible rupture with the release of nuclear factors. Recent progresses demonstrate that these mechanosensing processes lead to modulation of gene expression such as those involved in the regulation of cytoskeletal programs and introduce copy number variations. The nuclear lamina protein lamin A has a recurring role, and various biophysical analyses prove helpful in clarifying mechanisms. The various recent observations provide further motivation to understand the regulation of nuclear mechanosensing pathways in both physiological and pathological contexts.
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Cover Image
Cover Image
The image represents talin in focal adhesions. Talin is a mechanosensitive molecule that connects the integrin receptors in the cell membrane with the cytoskeleton. It is exposed to mechanical stretching, which induces the unfolding of its structure. This controls talin's interaction with other proteins, such as Deleted in Liver Cancer (DLC), which is a tumour suppressor and negative regulator of cell contractility. To learn more about this, please see the articles in this issue by Burridge (pages 673–675), Barnett and Kanchanawong (pages 677–680), and Popa and Berkovich (pages 687–699). The image was prepared by Magdalena von Essen, background picture: Vesa Hytönen.
Nuclear mechanosensing
Armando del Río Hernández, Yuntao Xia, Charlotte R. Pfeifer, Sangkyun Cho, Dennis E. Discher, Jerome Irianto; Nuclear mechanosensing. Emerg Top Life Sci 21 December 2018; 2 (5): 713–725. doi: https://doi.org/10.1042/ETLS20180051
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