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Cell Rep. 2016 Feb 16;14(6):1283-1292. doi: 10.1016/j.celrep.2016.01.035. Epub 2016 Feb 4.

5-Hydroxymethylcytosine Marks Sites of DNA Damage and Promotes Genome Stability.

Author information

1
Institute for Integrated Cell-Material Sciences (iCeMS), Kyoto University, Kyoto 606-8501, Japan; CREST, Japan Science and Technology Agency.
2
Institute for Integrated Cell-Material Sciences (iCeMS), Kyoto University, Kyoto 606-8501, Japan.
3
Laboratory of Genome Science, Biosignal Genome Resource Center, Institute for Molecular and Cellular Regulation, Gunma University, Maebashi, Gunma 371-8511, Japan.
4
Laboratory of Epigenetics, Institute for Protein Research, Osaka University, Suita, Osaka 565-0871, Japan; CREST, Japan Science and Technology Agency.
5
Laboratory of Epigenetics, Institute for Protein Research, Osaka University, Suita, Osaka 565-0871, Japan.
6
Institute for Integrated Cell-Material Sciences (iCeMS), Kyoto University, Kyoto 606-8501, Japan; CREST, Japan Science and Technology Agency. Electronic address: pcarlton@icems.kyoto-u.ac.jp.

Abstract

5-hydroxymethylcytosine (5hmC) is a DNA base created during active DNA demethylation by the recently discovered TET enzymes. 5hmC has essential roles in gene expression and differentiation. Here, we demonstrate that 5hmC also localizes to sites of DNA damage and repair. 5hmC accumulates at damage foci induced by aphidicolin and microirradiation and colocalizes with major DNA damage response proteins 53BP1 and γH2AX, revealing 5hmC as an epigenetic marker of DNA damage. Deficiency for the TET enzymes eliminates damage-induced 5hmC accumulation and elicits chromosome segregation defects in response to replication stress. Our results indicate that the TET enzymes and 5hmC play essential roles in ensuring genome integrity.

PMID:
26854228
DOI:
10.1016/j.celrep.2016.01.035
[Indexed for MEDLINE]
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