Nucleosome disassembly during human non-homologous end joining followed by concerted HIRA- and CAF-1-dependent reassembly. Academic Article uri icon

Overview

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.

publication date

  • June 8, 2016

Research

keywords

  • Cell Cycle Proteins
  • Chromatin Assembly Factor-1
  • DNA End-Joining Repair
  • Histone Chaperones
  • Nucleosomes
  • Transcription Factors

Identity

PubMed Central ID

  • PMC4915809

Scopus Document Identifier

  • 84975221884

Digital Object Identifier (DOI)

  • 10.1146/annurev.genet.40.110405.090451

PubMed ID

  • 27269284

Additional Document Info

volume

  • 5