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DDB2 promotes chromatin decondensation at UV-induced DNA damage

Luijsterburg, MS (author)
Lindh, M (author)
Acs, K (author)
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Vrouwe, MG (author)
Pines, A (author)
van Attikum, H (author)
Mullenders, LH (author)
Dantuma, NP (author)
Karolinska Institutet
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 (creator_code:org_t)
2012-04-09
2012
English.
In: The Journal of cell biology. - : Rockefeller University Press. - 1540-8140 .- 0021-9525. ; 197:2, s. 267-281
  • Journal article (peer-reviewed)
Abstract Subject headings
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  • Nucleotide excision repair (NER) is the principal pathway that removes helix-distorting deoxyribonucleic acid (DNA) damage from the mammalian genome. Recognition of DNA lesions by xeroderma pigmentosum group C (XPC) protein in chromatin is stimulated by the damaged DNA-binding protein 2 (DDB2), which is part of a CUL4A–RING ubiquitin ligase (CRL4) complex. In this paper, we report a new function of DDB2 in modulating chromatin structure at DNA lesions. We show that DDB2 elicits unfolding of large-scale chromatin structure independently of the CRL4 ubiquitin ligase complex. Our data reveal a marked adenosine triphosphate (ATP)–dependent reduction in the density of core histones in chromatin containing UV-induced DNA lesions, which strictly required functional DDB2 and involved the activity of poly(adenosine diphosphate [ADP]–ribose) polymerase 1. Finally, we show that lesion recognition by XPC, but not DDB2, was strongly reduced in ATP-depleted cells and was regulated by the steady-state levels of poly(ADP-ribose) chains.

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