Nucleosome disassembly during human non-homologous end joining followed by concerted HIRA- and CAF-1-dependent reassembly

  1. Xuan Li
  2. Jessica K Tyler  Is a corresponding author
  1. Weill Cornell Medicine, United States

Abstract

The cell achieves DNA double-strand break (DSB) repair in the context of chromatin structure. However, the mechanisms used to expose DSBs to the repair machinery and to restore the chromatin organization after repair remain elusive. Here we show that induction of a DSB in human cells causes local nucleosome disassembly, apparently independently from DNA end resection. This efficient removal of histone H3 from the genome during non-homologous end joining was promoted by both ATM and the ATP-dependent nucleosome remodeler INO80. Chromatin reassembly during DSB repair was dependent on the HIRA histone chaperone that is specific to the replication-independent histone variant H3.3 and on CAF-1 that is specific to the replication-dependent canonical histones H3.1/H3.2. Our data suggest that the epigenetic information is re-established after DSB repair by the concerted and interdependent action of replication-independent and replication-dependent chromatin assembly pathways.

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Author details

  1. Xuan Li

    Department of Pathology and Laboratory Medicine, Weill Cornell Medicine, New York, United States
    Competing interests
    No competing interests declared.
  2. Jessica K Tyler

    Department of Pathology and Laboratory Medicine, Weill Cornell Medicine, New York, United States
    For correspondence
    jet2021@med.cornell.edu
    Competing interests
    Jessica K Tyler, 'Senior editor, eLife.

Copyright

© 2016, Li & Tyler

This article is distributed under the terms of the Creative Commons Attribution License permitting unrestricted use and redistribution provided that the original author and source are credited.

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  1. Xuan Li
  2. Jessica K Tyler
(2016)
Nucleosome disassembly during human non-homologous end joining followed by concerted HIRA- and CAF-1-dependent reassembly
eLife 5:e15129.
https://doi.org/10.7554/eLife.15129

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https://doi.org/10.7554/eLife.15129