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Non-homologous end joining is important for repair of Cr(VI)-induced DNA damage in Saccharomyces cerevisiae

  1. Author:
    Santoyo, G.
    Strathern, J. N.
  2. Author Address

    Santoyo, Gustavo, Strathern, Jeffrey N.] NCI, Gene Regulat & Chromosome Biol Lab, NIH, Frederick, MD 21702 USA.
    1. Year: 2008
  1. Journal: Microbiological Research
    1. 163
    2. 1
    3. Pages: 113-119
  2. Type of Article: Article
  1. Abstract:

    Hexavalent chromium is known to be a potent carcinogen that leads to many different DNA lesions, including DNA - protein crosslinks, and single- and doubte-strand breaks. In Saccharomyces cerevisiae, DNA double-strand breaks are mainly repaired by either homologous recombination (HR) or non-homologous end-joining (NHEJ) repair pathways. Here, we show that mutants deficient in NHEJ (yku70 Delta, rad50 Delta, dnl4 Delta, mre11 Delta, xrs2 Delta) of S. cerevisiae are more sensitive to Cr(VI) toxic effects than wild-type cells. Also, a deletion mutant of SAE2 showed a similar sensitivity to Cr(VI), even though it has no apparent direct role in NHEJ. We also found that double mutants in HR and NHEJ (yku70 Delta/rad52 Delta, rad50 Delta/rad52 Delta, dnl4 Delta/rad52 Delta, mre11 Delta/rad52 Delta, xrs2 Delta/rad52 Delta) are synergistically more sensitive to Cr(VI) exposure than any of the single mutants, indicating that both repair pathways are involved in the repair of Cr(Vl)-induced lesions. Finally, when the NHEJ mutants were exposed to Cr(VI) under anaerobic growth conditions, Cr(VI) toxicity was suppressed. (c) 2007 Elsevier GmbH. All rights reserved.

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External Sources

  1. PMID: 17923397

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