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Article

Mechanotransduction via the LINC complex regulates DNA replication in myonuclei

View ORCID ProfileShuoshuo Wang, Elizabeth Stoops, View ORCID ProfileUnnikannan CP, Barak Markus, Adriana Reuveny, Elly Ordan, View ORCID ProfileTalila Volk  Correspondence email
Shuoshuo Wang
Department of Molecular Genetics, Weizmann Institute of Science, Rehovot, Israel
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Elizabeth Stoops
Department of Molecular Genetics, Weizmann Institute of Science, Rehovot, Israel
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Unnikannan CP
Department of Molecular Genetics, Weizmann Institute of Science, Rehovot, Israel
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Barak Markus
G-INCPM/Mantoux Institute for Bioinformatics, Weizmann Institute of Science, Rehovot, Israel
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Adriana Reuveny
Department of Molecular Genetics, Weizmann Institute of Science, Rehovot, Israel
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Elly Ordan
Department of Molecular Genetics, Weizmann Institute of Science, Rehovot, Israel
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Talila Volk
Department of Molecular Genetics, Weizmann Institute of Science, Rehovot, Israel
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  • For correspondence: Talila.volk@weizmann.ac.il
DOI: 10.1083/jcb.201708137 | Published April 12, 2018
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Abstract

Nuclear mechanotransduction has been implicated in the control of chromatin organization; however, its impact on functional contractile myofibers is unclear. We found that deleting components of the linker of nucleoskeleton and cytoskeleton (LINC) complex in Drosophila melanogaster larval muscles abolishes the controlled and synchronized DNA endoreplication, typical of nuclei across myofibers, resulting in increased and variable DNA content in myonuclei of individual myofibers. Moreover, perturbation of LINC-independent mechanical input after knockdown of β-Integrin in larval muscles similarly led to increased DNA content in myonuclei. Genome-wide RNA-polymerase II occupancy analysis in myofibers of the LINC mutant klar indicated an altered binding profile, including a significant decrease in the chromatin regulator barrier-to-autointegration factor (BAF) and the contractile regulator Troponin C. Importantly, muscle-specific knockdown of BAF led to increased DNA content in myonuclei, phenocopying the LINC mutant phenotype. We propose that mechanical stimuli transmitted via the LINC complex act via BAF to regulate synchronized cell-cycle progression of myonuclei across single myofibers.

  • Submitted: 21 August 2017
  • Revision received 8 February 2018
  • Accepted: 27 March 2018
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This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.rupress.org/terms/). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 4.0 International license, as described at https://creativecommons.org/licenses/by-nc-sa/4.0/).

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© 2018 Wang et al. http://www.rupress.org/terms/https://creativecommons.org/licenses/by-nc-sa/4.0/This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.rupress.org/terms/). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 4.0 International license, as described at https://creativecommons.org/licenses/by-nc-sa/4.0/).

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Mechanotransduction via the LINC complex regulates DNA replication in myonuclei
Shuoshuo Wang, Elizabeth Stoops, Unnikannan CP, Barak Markus, Adriana Reuveny, Elly Ordan, Talila Volk
J Cell Biol Apr 2018, jcb.201708137; DOI: 10.1083/jcb.201708137

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The Journal of Cell Biology: 217 (4)

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April 2, 2018
Volume 217, No. 4

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