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Nucleotide excision repair/TFIIH helicases Rad3 and Ssl2 inhibit short-sequence recombination and Ty1 retrotransposition by similar mechanisms

  1. Author:
    Lee, B. S.
    Bi, L.
    Garfinkel, D. J.
    Bailis, A. M.

  2. Author Address

    Garfinkel DJ NCI, Gene Regulat & Chromosome Biol Lab, Frederick Canc Res & Dev Ctr, NIH POB B Frederick, MD 21702 USA NCI, Gene Regulat & Chromosome Biol Lab, Frederick Canc Res & Dev Ctr, NIH Frederick, MD 21702 USA City Hope Natl Med Ctr, Beckman Res Inst, Dept Mol Biol Duarte, CA 91010 USA
    1. Year: 2000
  2. Journal: Molecular and Cellular Biology
    1. 20
    2. 7
    3. Pages: 2436-2445
  4. Type of Article: Article
  1. Abstract:

    Eukaryotic genomes contain potentially unstable sequences whose rearrangement threatens genome structure and function. Here we show that certain mutant alleles of the nucleotide excision repair (NER)/TFIIH helicase genes RAD3 and SSL2 (RAD25) confer synthetic lethality and destabilize the Saccharomyces cerevisiae genome by increasing both short-sequence recombination and Ty1 retrotransposition. The rad3-G595R and ssl1-rtt mutations do not markedly alter Ty1 RNA or protein levels or target site specificity. However, these mutations cause an increase in the physical stability of broken DNA molecules and unincorporated Ty1 cDNA, which leads to higher levels of short-sequence recombination and Ty1 retrotransposition. Our results link components of the core NER/TFIIH complex with genome stability, homologous recombination, and host defense against Ty1 retrotransposition via a mechanism that involves DNA degradation. [References: 77]

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