Effect of DNA lesions on transcription elongation

Some types of damage to cellular DNA have been shown to interfere with the essential transactions of replication and transcription. Not only may the translocation of the polymerase be arrested at the site of the lesion but the bound protein may encumber recognition of the lesion by repair enzymes. In the case of transcription a subpathway of excision repair, termed transcription-coupled repair (TCR) has been shown to operate on lesions in the transcribed strands of expressed genes in bacteria, yeast, mammalian cells and a number of other organisms. Certain genes in mammalian cells (e.g., CSA and CSB) have been uniquely implicated in TCR while others (e.g., XPC-HR23 and XPE) have been shown to operate in the global genomic pathway of nucleotide excision repair, but not in TCR. In order to understand the mechanism of TCR it is important to learn how an RNA polymerase elongation complex interacts with a damaged DNA template. That relationship is explored for different lesions and different RNA polymerase systems in this article.