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Physicochemical mechanotransduction alters nuclear shape and mechanics via heterochromatin formation

Andrew D. Stephens, Patrick Z. Liu, Viswajit Kandula, Haimei Chen, Luay M. Almassalha, Vadim Backman, Thomas O’Halloran, Stephen A. Adam, Robert D. Goldman, Edward J. Banigan, John F. Marko
doi: https://doi.org/10.1101/423442
Andrew D. Stephens
1Department of Molecular Biosciences, Northwestern University, Evanston, IL 60208
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  • For correspondence: andrew.stephens@northwestern.edu
Patrick Z. Liu
1Department of Molecular Biosciences, Northwestern University, Evanston, IL 60208
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Viswajit Kandula
1Department of Molecular Biosciences, Northwestern University, Evanston, IL 60208
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Haimei Chen
2Department of Chemistry, Northwestern University, Evanston, IL 60208
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Luay M. Almassalha
3Department of Biomedical Engineering, Northwestern University, Evanston, IL 60208
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Vadim Backman
3Department of Biomedical Engineering, Northwestern University, Evanston, IL 60208
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Thomas O’Halloran
2Department of Chemistry, Northwestern University, Evanston, IL 60208
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Stephen A. Adam
4Department of Cell and Molecular Biology, Northwestern University Feinberg School of Medicine, Chicago, IL 60611
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Robert D. Goldman
4Department of Cell and Molecular Biology, Northwestern University Feinberg School of Medicine, Chicago, IL 60611
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Edward J. Banigan
5Institute for Medical Engineering and Science, Massachusetts Institute of Technology, Cambridge, MA 02139
6Department of Physics and Astronomy, Northwestern University, Evanston, IL 60208
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John F. Marko
1Department of Molecular Biosciences, Northwestern University, Evanston, IL 60208
6Department of Physics and Astronomy, Northwestern University, Evanston, IL 60208
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Abstract

The nucleus houses, organizes, and protects chromatin to ensure genome integrity and proper gene expression, but how the nucleus adapts mechanically to changes in the extracellular environment is poorly understood. Recent studies have revealed that extracellular chemical or physical stresses induce chromatin compaction via mechanotransductive processes. We report that increased extracellular multivalent cations lead to increased heterochromatin levels through mechanosensitive ion channels. This increase in heterochromatin results in increased chromatin-based nuclear rigidity, which suppresses nuclear blebbing in cells with perturbed chromatin or lamins. Furthermore, transduction of elevated extracellular cations rescues nuclear morphology in model and patient cells of human diseases, including progeria and the breast cancer model cell line MDA-MB-231. We conclude that nuclear mechanics and morphology, including abnormal phenotypes found in human diseases, can be modulated by cell sensing of the extracellular environment and consequent changes to histone modification state and chromatin-based nuclear rigidity, without requiring direct mechanical perturbations to the cell interior.

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The copyright holder for this preprint is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under a CC-BY-NC 4.0 International license.
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Posted September 21, 2018.
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Physicochemical mechanotransduction alters nuclear shape and mechanics via heterochromatin formation
Andrew D. Stephens, Patrick Z. Liu, Viswajit Kandula, Haimei Chen, Luay M. Almassalha, Vadim Backman, Thomas O’Halloran, Stephen A. Adam, Robert D. Goldman, Edward J. Banigan, John F. Marko
bioRxiv 423442; doi: https://doi.org/10.1101/423442
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Physicochemical mechanotransduction alters nuclear shape and mechanics via heterochromatin formation
Andrew D. Stephens, Patrick Z. Liu, Viswajit Kandula, Haimei Chen, Luay M. Almassalha, Vadim Backman, Thomas O’Halloran, Stephen A. Adam, Robert D. Goldman, Edward J. Banigan, John F. Marko
bioRxiv 423442; doi: https://doi.org/10.1101/423442

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