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Molecular and Cellular Biology, February 2003, p. 1453-1459, Vol. 23, No. 4
0270-7306/03/$08.00+0     DOI: 10.1128/MCB.23.4.1453-1459.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.

Yeast DNA Polymerase {zeta} Is an Efficient Extender of Primer Ends Opposite from 7,8-Dihydro-8-Oxoguanine and O6-Methylguanine

Lajos Haracska, Satya Prakash, and Louise Prakash*

Sealy Center for Molecular Science, University of Texas Medical Branch, Galveston, Texas 77555-1061

Received 26 September 2002/ Returned for modification 31 October 2002/ Accepted 18 November 2002

Genetic studies in Saccharomyces cerevisiae have indicated the requirement of DNA polymerase (Pol) {zeta} for mutagenesis induced by UV light and by other DNA damaging agents. However, on its own, Pol{zeta} is highly inefficient at replicating through DNA lesions; rather, it promotes their mutagenic bypass by extending from the nucleotide inserted opposite the lesion by another DNA polymerase. So far, such a role for Pol{zeta} has been established for cyclobutane pyrimidine dimers, (6-4) dipyrimidine photoproducts, and abasic sites. Here, we examine whether Pol{zeta} can replicate through the 7,8-dihydro-8-oxoguanine (8-oxoG) and O6-methylguanine (m6G) lesions. We chose these two lesions for this study because the replicative polymerase, Pol{delta}, can replicate through them, albeit weakly. We found that Pol{zeta} is very inefficient at inserting nucleotides opposite both these lesions, but it can efficiently extend from the nucleotides inserted opposite them by Pol{delta}. Also, the most efficient bypass of 8-oxoG and m6G lesions occurs when Pol{delta} is combined with Pol{zeta}, indicating a role for Pol{zeta} in extending from the nucleotides inserted opposite these lesions by Pol{delta}. Thus, Pol{zeta} is a highly specialized polymerase that can proficiently extend from the primer ends opposite DNA lesions, irrespective of their degree of geometric distortion. Pol{zeta}, however, is unusually sensitive to geometric distortion of the templating residue, as it is highly inefficient at incorporating nucleotides even opposite the moderately distorting 8-oxoG and m6G lesions.

* Corresponding author. Mailing address: Sealy Center for Molecular Science, University of Texas Medical Branch, 6.104 Blocker Medical Research Building, 11th and Mechanic Streets, Galveston, TX 77555-1061. Phone: (409) 747-8601. Fax: (409) 747-8608. E-mail: l.prakash{at}utmb.edu.

Molecular and Cellular Biology, February 2003, p. 1453-1459, Vol. 23, No. 4
0022-538X/03/$08.00+0     DOI: 10.1128/MCB.23.4.1453-1459.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.



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