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    DNA Repair (Amst). 2006 Feb 3;5(2):226-34. Epub 2005 Nov 11.

    The effect of oxidative metabolism on spontaneous Pol zeta-dependent translesion synthesis in Saccharomyces cerevisiae.

    Minesinger BK, Abdulovic AL, Ou TM, Jinks-Robertson S.

    Source

    Biochemistry, Cell and Developmental Biology Program of the Graduate Division of Biological and Biomedical Sciences, Emory University, Atlanta, GA 30322, USA.

    Abstract

    DNA lesions can stall or block high-fidelity polymerases, thus inhibiting replication. To bypass such lesions, low-fidelity translesion synthesis (TLS) polymerases can be used to insert a nucleotide across from the lesion or extend from a lesion:base mispair. When DNA repair is compromised in Saccharomyces cerevisiae, spontaneous DNA lesions can lead to a novel mutational event in which a frameshift is accompanied by one or more base pair substitutions. These "complex frameshifts" are dependent upon the TLS polymerase Pol zeta, and provide a mutational signature for mutagenic Pol zeta-dependent activity. In the current study, we have found that a specific subset of the Pol zeta-dependent mutational events requires oxidative metabolism. These results suggest that translesion bypass of spontaneously oxidized DNA bases can be a significant source of mutagenesis in repair compromised cells.

    PMID:
    16290107
    [PubMed - indexed for MEDLINE]

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