Journal
NUCLEIC ACIDS RESEARCH
Volume 32, Issue 15, Pages 4665-4675Publisher
OXFORD UNIV PRESS
DOI: 10.1093/nar/gkh777
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Funding
- NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES [Z01ES065070, ZIAES065070, Z01ES065046] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF GENERAL MEDICAL SCIENCES [R01GM058534, R01GM032431] Funding Source: NIH RePORTER
- NIGMS NIH HHS [R01 GM032431, GM58534, R01 GM058534] Funding Source: Medline
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When cyclobutane pyrimidine dimers stall DNA replication by DNA polymerase (Pol) delta or epsilon, a switch occurs to allow translesion synthesis by DNA polymerase eta, followed by another switch that allows normal replication to resume. In the present study, we investigate these switches using Saccharomyces cerevisiae Pol delta, Pol epsilon and Pol eta and a series of matched and mismatched primer templates that mimic each incorporation needed to completely bypass a cis-syn thymine-thymine (TT) dimer. We report a complementary pattern of substrate use indicating that enzymatic switching involving localized translesion synthesis by Pol eta and mismatch excision and polymerization by a major replicative polymerase can account for the efficient and accurate dimer bypass known to suppress sunlight-induced mutagenesis and skin cancer.
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