کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
1981519 | 1061950 | 2006 | 9 صفحه PDF | دانلود رایگان |

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 Polζ, and provide a mutational signature for mutagenic Polζ-dependent activity. In the current study, we have found that a specific subset of the Polζ-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.
Journal: DNA Repair - Volume 5, Issue 2, 3 February 2006, Pages 226–234