UV light-induced DNA damage and tolerance for the survival of nucleotide excision repair-deficient human cells

Satoshi Nakajima, Li Lan, Shin Ichiro Kanno, Masashi Takao, Kazuo Yamamoto, Andre P.M. Eker, Akira Yasui

研究成果: Article査読

63 被引用数 (Scopus)

抄録

DNA damage can cause cell death unless it is either repaired or tolerated. The precise contributions of repair and tolerance mechanisms to cell survival have not been previously evaluated. Here we have analyzed the cell killing effect of the two major UV light-induced DNA lesions, cyclobutane pyrimidine dimers (CPDs) and 6-4 pyrimidine-pyrimidone photoproducts (6-4PPs), in nucleotide excision repair-deficient human cells by expressing pliotolyase(s) for light-dependent photorepair of either or both lesions. Immediate repair of the less abundant 6-4PPs enhances the survival rate to a similar extent as the immediate repair of CPDs, indicating that a single 6-4PP lesion is severalfold more toxic than a CPD in the cells. Because UV light-induced DNA damage is not repaired at all in nucleotide excision repair-deficient cells, proliferation of these cells after UV light irradiation must be achieved by tolerance of the damage at replication. We found that RNA interference designed to suppress polymerase ζ activity made the cells more sensitive to UV light. This increase in sensitivity was prevented by photorepair of 6-4PPs but not by photorepair of CPDs, indicating that polymerase ζ is involved in the tolerance of 6-4PPs in human cells.

本文言語English
ページ(範囲)46674-46677
ページ数4
ジャーナルJournal of Biological Chemistry
279
45
DOI
出版ステータスPublished - 2004 11 5

ASJC Scopus subject areas

  • Biochemistry
  • Molecular Biology
  • Cell Biology

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