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M208169200v1
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Papers In Press, published online ahead of print September 10, 2002
J. Biol. Chem, 10.1074/jbc.M208169200
Submitted on August 9, 2002
Revised on September 5, 2002
Accepted on September 10, 2002

Saccharomyces cerevisiae RAD5 influences the excision repair of DNA minor groove adducts

Konstantinos Kiakos, Tiffany T. Howard, Moses Lee, John A. Hartley, and Peter J. McHugh

Cancer Research UK Laboratories, Weatherall Institute of Molecular Medicine, Oxford, Oxon OX3 9DS

Corresponding Author: peter.mchugh{at}cancer.org.uk

Nucleotide excision repair (NER) is the primary pathway for the removal of DNA adducts which distort the double helix. In the yeast Saccharomyces cerevisiae the RAD6 epistasis group defines a more poorly characterised set of DNA damage response pathways, believed to be distinct from NER. Here we show that the elimination of the DNA minor groove adducts formed by an important class of anticancer antibiotic (CC-1065 family) requires NER factors in S. cerevisiae. We also demonstrate that the elimination of this class of minor groove adduct from the active MFA2 gene depends upon functional Rad18 and Rad6. This is most clear for the repair of adducts on the transcribed strand, where an absolute requirement for Rad6 and Rad18 was seen. Further experiments revealed that a specific RAD6-RAD18 controlled subpathway, the RAD5 branch, mediates these events. Cells disrupted for rad5 are highly sensitive to this minor groove binding agent and rad5 cells exhibit an in vivo adduct elimination defect indistinguishable from that seen in rad6 and rad18 cells, as well as NER defective cells. Our results indicate that the RAD5 subpathway may interact with NER factors during the repair of certain DNA adducts.


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