CPD damage recognition by transcribing RNA polymerase II
2007 | journal article; research paper. A publication with affiliation to the University of Göttingen.
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- Authors
- Brueckner, Florian; Hennecke, Ulrich; Carell, Thomas; Cramer, Patrick
- Abstract
- Cells use transcription-coupled repair (TCR) to efficiently eliminate DNA lesions such as ultraviolet light-induced cyclobutane pyrimidine dimers (CPDs). Here we present the structure-based mechanism for the first step in eukaryotic TCR, CPD-induced stalling of RNA polymerase (Pol)II. A CPD in the transcribed strand slowly passes a translocation barrier and enters the polymerase active site. The CPD 5'-thymine then directs uridine misincorporation into messenger RNA, which blocks translocation. Artificial replacement of the uridine by adenosine enables CPD bypass; thus, Pol II stalling requires CPD-directed misincorporation. In the stalled complex, the lesion is inaccessible, and the polymerase conformation is unchanged. This is consistent with nonallosteric recruitment of repair factors and excision of a lesion-containing DNA fragment in the presence of Pol II.
- Issue Date
- 2007
- Journal
- Science
- ISSN
- 0036-8075
- Language
- English