|
||
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Report |
Heterochromatin protein 1 is recruited to various types of DNA damage
Correspondence to Roel van Driel: r.vandriel{at}uva.nl
Heterochromatin protein 1 (HP1) family members are chromatin-associated proteins involved in transcription, replication, and chromatin organization. We show that HP1 isoforms HP1-
, HP1-β, and HP1-
are recruited to ultraviolet (UV)-induced DNA damage and double-strand breaks (DSBs) in human cells. This response to DNA damage requires the chromo shadow domain of HP1 and is independent of H3K9 trimethylation and proteins that detect UV damage and DSBs. Loss of HP1 results in high sensitivity to UV light and ionizing radiation in the nematode Caenorhabditis elegans, indicating that HP1 proteins are essential components of DNA damage response (DDR) systems. Analysis of single and double HP1 mutants in nematodes suggests that HP1 homologues have both unique and overlapping functions in the DDR. Our results show that HP1 proteins are important for DNA repair and may function to reorganize chromatin in response to damage.
Abbreviations used in this paper: CD, chromodomain; CSB, Cockayne syndrome protein B; CSD, chromo shadow domain; DDR, DNA damage response; DSB, double-strand break; FLIP, fluorescence loss in photobleaching; FP, fluorescent protein; GGR, global genome NER; HP1, heterochromatin protein 1; IR, ionizing radiation; mRFP, monomeric RFP; NER, nucleotide excision repair; NHEJ, nonhomologous end joining; PCNA, proliferating cell nuclear antigen; SCFP, super cyan FP; TCR, transcription-coupled NER; XP, xeroderma pigmentosum.
© 2009 Luijsterburg et al.
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.jcb.org/misc/terms.shtml). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 3.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/3.0/).
Related Article
This article has been cited by other articles:
|
|