Format

Send to

Choose Destination
Elife. 2016 Jun 8;5. pii: e15129. doi: 10.7554/eLife.15129.

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

Author information

1
Department of Pathology and Laboratory Medicine, Weill Cornell Medicine, New York, 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.

KEYWORDS:

DSB repair; H3.3; NHEJ; assembly; chromatin; chromosomes; disassembly; genes; human

PMID:
27269284
PMCID:
PMC4915809
DOI:
10.7554/eLife.15129
[Indexed for MEDLINE]
Free PMC Article

Supplemental Content

Full text links

Icon for eLife Sciences Publications, Ltd Icon for PubMed Central
Loading ...
Support Center