Toward an Understanding of Nucleotide Excision Repair in Yeast: A Summary of Recent Progress

  • Louie Naumovski
  • Wolfram Siede
  • William A. Weiss
  • Errol C. Friedberg


With its established classical and molecular genetics, and emerging biochemistry, the yeast Saccharoamyyces cerevisiae is an ideal organism in which to study eukaryotic DNA metabolism. The excision repair of DNA damage in yeast is a complex process, controlled by a number of different genes in the so-called RAD3 epistasis group. Mutations at any of approximately 12 independent loci in this epistasis group cause cells to become abnormally sensitive to killing by ultraviolet light on or DNA damaging chemicals (for recent reviews on DNA repair in yeast see Haynes and Kunz, 1981 and Friedberg, 1988). For 5 of these loci (RAD1, RAD2, RAD3, RAD4 and RAD10) mutations completely block the ability of cells to incise DNA in response to damage (Reynolds and Friedberg, 1981; Wilcox and Prakash, 1981). In the other 7 genes (RAD7, RAD14, RAD16, RAD23, RAD24, CDC8 and MMS19) mutations impair, but do not completely block this process. It is the goal of this and of other laboratories to clone the yeast genes involved in excision repair, with particular emphasis on the 5 genes which appear to be absolutely required for this process. The cloned genes can then be used to overexpress and purify specific Rad proteins, and hence to attempt to understand the biochemistry of eukaryotic nucleotide excision repair.


ATPase Activity Excision Repair Repair Gene Nucleotide Excision Repair Rad4 Mutant 
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Copyright information

© Springer Science+Business Media New York 1989

Authors and Affiliations

  • Louie Naumovski
    • 1
  • Wolfram Siede
    • 1
  • William A. Weiss
    • 1
  • Errol C. Friedberg
    • 1
  1. 1.Department of PathologyStanford University School of MedicineStanfordUSA

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