A mouse kidney cell line with a G:C → C:G transversion mutator phenotype

Chi Y. Shin, Olga N. Ponomareva, Lanelle Connolly, Mitchell S. Turker

Research output: Contribution to journalArticle

8 Scopus citations

Abstract

We report the identification of a mouse kidney epithelial cell line (K435) in which G:C→C:G transversion mutations occur at an elevated rate and are the predominant spontaneous events observed at the selectable Aprt locus. Of three genotoxins tested, ultraviolet radiation (UV), ionizing radiation, and hydrogen peroxide, only UV exposure was able to alter the spectrum of small mutational events. To determine if the G:C→C:G mutator phenotype was due to a deficiency in the mismatch repair pathway, the K435 cells were tested for resistance to 6-thioguanine, cisplatin, and MNNG. Although the K435 cells were as resistant to 6-thioguanine and cisplatin as Pms2 and Mlh1 null kidney cells, they were hypersensitive to MNNG. Moreover, the K435 cells do not exhibit microsatellite instability, a hallmark of mismatch repair deficiency. These results suggest that a novel mechanism, which does not include a classical deficiency in mismatch repair, accounts for the G:C→C:G mutator phenotype.

Original languageEnglish (US)
Pages (from-to)69-76
Number of pages8
JournalMutation Research - Fundamental and Molecular Mechanisms of Mutagenesis
Volume503
Issue number1-2
DOIs
StatePublished - Jan 1 2002

Keywords

  • DNA mismatch repair
  • Drug resistance
  • Mutator phenotype
  • Transversion mutation

ASJC Scopus subject areas

  • Molecular Biology
  • Genetics
  • Health, Toxicology and Mutagenesis

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