WRN functions in a RAD18-dependent damage avoidance pathway

Yu Peng Dong, Masayuki Seki, Akari Yoshimura, Eri Inoue, Shinya Furukawa, Shusuke Tada, Takemi Enomoto

Research output: Contribution to journalArticlepeer-review

10 Citations (Scopus)


Werner syndrome (WS), caused by mutations in a gene (WRN) that encodes a RecQ DNA helicase, is characterized by premature aging and cancer predisposition. Cells derived from WS patients show sensitivity to several DNA damaging agents. Previous studies revealed that the WRN protein plays roles in DNA repair or damage tolerance, although it was not yet assigned to a specific pathway. Here we examined the relationship between WRN and the post-replication repair protein RAD18 by generating deletion derivatives in chicken DT40 cells. The frequency of spontaneous sister chromatid exchange in WRN -/-/RAD18-/- double mutant cells was slightly increased compared to that of either single mutant. However, the sensitivity of WRN -/-/RAD18-/- cells to 4-nitroquinoline 1-oxide and methyl methanesulfonate was almost the same as that of RAD18-/- cells. Moreover, the cisplatin sensitivity of RAD18-/- cells was slightly suppressed by disruption of WRN. These data suggest that WRN functions in a pathway involving RAD18 under damage-inducing conditions.

Original languageEnglish
Pages (from-to)1080-1083
Number of pages4
JournalBiological and Pharmaceutical Bulletin
Issue number6
Publication statusPublished - 2007 Jun


  • DT40
  • Maintenance of genome stability 1 (Mgs1)
  • Proliferating cell nuclear antigen (PCNA)
  • RAD18
  • RecQ
  • Werner syndrome (WRN)

ASJC Scopus subject areas

  • Pharmacology
  • Pharmaceutical Science


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