Age-dependent spontaneous mutagenesis in Xpc mice defective in nucleotide excision repair

Susan W P Wijnhoven, Hanneke J M Kool, Leon H F Mullenders, Albert A. Van Zeeland, Errol C. Friedberg, Gijsbertus T J Van Der Horst, Harry Van Steeg, Harry Vrieling

Research output: Contribution to journalArticlepeer-review

53 Scopus citations


DNA damages caused by cellular metabolites and environmental agents induce mutations, that may predispose to cancer. Nucleotide excision repair (NER) is a major cellular defence mechanism acting on a variety of DNA lesions. Here, we show that spontaneous mutant frequencies at the Hprt gene increased 30-fold in T-lymphocytes of 1 year old Xpc(-/-) mice, possessing only functional transcription-coupled repair (TCR). Hprt mutant frequencies in Xpa(-/-) and Csb(-/-) mice that both have a defect in this NER subpathway, remained low during ageing. In contrast to current models, the elevated mutation rate in Xpc(-/-) mice does not lead to an increased tumour incidence or premature ageing.

Original languageEnglish (US)
Pages (from-to)5034-5037
Number of pages4
Issue number43
StatePublished - Oct 12 2000


  • Cancer
  • Hprt
  • Mutation
  • Nucleotide excision repair
  • Transgenic mice

ASJC Scopus subject areas

  • Molecular Biology
  • Genetics
  • Cancer Research


Dive into the research topics of 'Age-dependent spontaneous mutagenesis in Xpc mice defective in nucleotide excision repair'. Together they form a unique fingerprint.

Cite this