Jump to main content
Jump to site search
PLANNED MAINTENANCE Close the message box

Scheduled maintenance upgrade on Thursday 4th of May 2017 from 8.00am to 9.00am (BST).

During this time our websites will be offline temporarily. If you have any questions please use the feedback button on this page. We apologise for any inconvenience this might cause and thank you for your patience.


Issue 6, 2012
Previous Article Next Article

Mechanism of UV-induced Dewar lesion repair catalysed by DNA (6-4) photolyase

Author affiliations

Abstract

UV irradiation of cellular DNA leads to the formation of mutagenic pyrimidine derived dimer lesions. One of the stable end products of the lesion forming pathways are DNA Dewar lesions. Here we report that the TpC derived Dewar lesions are efficiently repaired by the repair enzyme (6-4) photolyase, while the TpT derived Dewar lesion is unrepairable. We provide experimental and theoretical data showing that the substituent of the Dewar substructure is mainly responsible for this behavior. Studies with synthetic derivatives of the Dewar lesions and theory reveal how the substitution pattern of the important Dewar lesions governs their reparability.

Graphical abstract: Mechanism of UV-induced Dewar lesion repair catalysed by DNA (6-4) photolyase

Back to tab navigation
Please wait while Download options loads

Supplementary files

Publication details

The article was received on 30 Jan 2012, accepted on 02 Apr 2012 and first published on 02 Apr 2012


Article type: Edge Article
DOI: 10.1039/C2SC20122D
Citation: Chem. Sci., 2012,3, 1794-1797
  •   Request permissions

    Mechanism of UV-induced Dewar lesion repair catalysed by DNA (6-4) photolyase

    B. P. Fingerhut, K. Heil, E. Kaya, S. Oesterling, R. de Vivie-Riedle and T. Carell, Chem. Sci., 2012, 3, 1794
    DOI: 10.1039/C2SC20122D

Search articles by author