Format

Send to:

Choose Destination
See comment in PubMed Commons below
Cell Rep. 2014 May 22;7(4):1320-32. doi: 10.1016/j.celrep.2014.04.002. Epub 2014 May 9.

Isolation of chromatin from dysfunctional telomeres reveals an important role for Ring1b in NHEJ-mediated chromosome fusions.

Author information

  • 1Department of Molecular and Experimental Medicine, The Scripps Research Institute, La Jolla, CA 92037, USA.
  • 2Department of Chemical Physiology, The Scripps Research Institute, La Jolla, CA 92037, USA.
  • 3Department of Experimental Oncology, European Institute of Oncology, 20146 Milan, Italy.
  • 4Department of Molecular and Experimental Medicine, The Scripps Research Institute, La Jolla, CA 92037, USA. Electronic address: edenchi@scripps.edu.

Abstract

When telomeres become critically short, DNA damage response factors are recruited at chromosome ends, initiating a cellular response to DNA damage. We performed proteomic isolation of chromatin fragments (PICh) in order to define changes in chromatin composition that occur upon onset of acute telomere dysfunction triggered by depletion of the telomere-associated factor TRF2. This unbiased purification of telomere-associated proteins in functional or dysfunctional conditions revealed the dynamic changes in chromatin composition that take place at telomeres upon DNA damage induction. On the basis of our results, we describe a critical role for the polycomb group protein Ring1b in nonhomologous end-joining (NHEJ)-mediated end-to-end chromosome fusions. We show that cells with reduced levels of Ring1b have a reduced ability to repair uncapped telomeric chromatin. Our data represent an unbiased isolation of chromatin undergoing DNA damage and are a valuable resource to map the changes in chromatin composition in response to DNA damage activation.

Copyright © 2014 The Authors. Published by Elsevier Inc. All rights reserved.

PMID:
24813883
[PubMed - indexed for MEDLINE]
PMCID:
PMC4054697
Free PMC Article
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Elsevier Science Icon for PubMed Central
    Loading ...
    Write to the Help Desk