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RAD6–RAD18–RAD5-pathway-dependent tolerance to chronic low-dose ultraviolet light

Author

Listed:
  • Takashi Hishida

    (Research Institute for Microbial Diseases, Osaka University, 3-1 Yamadaoka, Suita, Osaka 565-0871, Japan)

  • Yoshino Kubota

    (Research Institute for Microbial Diseases, Osaka University, 3-1 Yamadaoka, Suita, Osaka 565-0871, Japan)

  • Antony M. Carr

    (MRC Genome Damage and Stability Centre, University of Sussex)

  • Hiroshi Iwasaki

    (International Graduate School of Arts and Sciences, Yokohama City University, 1-7-29, Suehiro, Tsurumi, Yokohama, Kanagawa 230-0045, Japan)

Abstract

DNA repair in real life Laboratories routinely expose cells to high doses of ultraviolet (UV) light to measure the response to DNA damage. But what happens in the real world, where organisms are exposed either continuously or intermittently to low levels of UV? A study of the effects of environmentally relevant UV levels on yeast cells shows that there is a DNA system sufficiently sensitive to kick in following low-UV exposure. It is the RAD6–RAD8–RAD5 post-replication repair pathway. By preventing the generation of excess single-stranded DNA when replication forks are interrupted, it allows cells to replicate their DNA when it is damaged, thereby avoiding the activation of a cellular response that would inhibit proliferation.

Suggested Citation

  • Takashi Hishida & Yoshino Kubota & Antony M. Carr & Hiroshi Iwasaki, 2009. "RAD6–RAD18–RAD5-pathway-dependent tolerance to chronic low-dose ultraviolet light," Nature, Nature, vol. 457(7229), pages 612-615, January.
    • Handle: RePEc:nat:nature:v:457:y:2009:i:7229:d:10.1038_nature07580
    DOI: 10.1038/nature07580
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