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CPD damage recognition by transcribing RNA polymerase II.

Brueckner F, Hennecke U, Carell T, Cramer P
Science 315 859-62 (2007)
Related entries: 2ja5, 2ja6, 2ja7

Cited: 150 times
EuropePMC logo PMID: 17290000

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.

Reviews - 2ja8 mentioned but not cited (1)

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Articles - 2ja8 mentioned but not cited (2)

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