ArticleProceedings of the National Academy of Sciences of the United States of America2000
The Dewar photoproduct of thymidylyl(3'-->5')- thymidine (Dewar product) exhibits mutagenic behavior in accordance with the "A rule".
Article in Proceedings of the National Academy of Sciences of the United States of America, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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4 citing papers in PubMed.
- Both DNA global deformation and repair enzyme contacts mediate flipping of thymine dimer damage.Scientific reports · 2017Article
- Surviving the sun: repair and bypass of DNA UV lesions.Protein science : a publication of the Protein Society · 2011Review
- Molecular mechanisms of ultraviolet radiation-induced DNA damage and repair.Journal of nucleic acids · 2010Article
- NMR structure of the DNA decamer duplex containing double T*G mismatches of cis-syn cyclobutane pyrimidine dimer: implications for DNA damage recognition by the XPC-hHR23B complex.Nucleic acids research · 2004Article
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3 authors.
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Abstract
In contrast to the highly mutagenic pyrimidine(6-4)pyrimidone photoproduct, its Dewar valence isomer (Dewar product) has low mutagenic potential and produces a broad range of mutations [LeClerc, J. E., Borden, A. & Lawrence, C. W. (1991) Proc. Natl. Acad. Sci. USA 88, 9685-9689]. To determine the origin of the mutagenic property of the Dewar product, we used experimental NMR restraints and molecular dynamics to determine the solution structure of a Dewar-lesion DNA decamer duplex. This DNA decamer duplex (DW/GA duplex) contains a mismatched base pair between the 3' T residue of the Dewar lesion (T6) and an opposed G residue (G15). The 3' T (T6) of the Dewar lesion formed stable hydrogen bonds with the opposing G15 residue. However, the helical bending and unwinding angles of the DW/GA duplex were much larger than those of a second duplex that contains the Dewar lesion and opposing A15 and A16 residues (DW/AA duplex). The DW/GA duplex showed poorer stacking interactions at the two bases of the Dewar product and at the adjacent A7 small middle dotT14 base pair than did the DW/AA duplex. These structural features imply that no thermal stability or conformational benefit is obtained by incorporating a G instead of an A opposite the 3' T of the Dewar lesion. These properties may thus facilitate the preferential incorporation of an A in accordance with the A rule during translesion replication and lead to the low frequency of 3' T-->C mutations observed at this site.
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