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doi: 10.1242/10.1242/jcs.00271

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Rescue of arrested RNA polymerase II complexes

Cancer Research UK London Research Institute, Clare Hall Laboratories, South Mimms, Hertfordshire EN6 3LD, UK

(e-mail: j.svejstrup{at}cancer.org.uk)

In the past few months, several discoveries relating to the mechanism underlying transcription-coupled DNA repair (TCR) have been reported. These results make it timely to propose a hypothesis for how eukaryotic cells might deal with arrested RNA polymerase II (Pol II) complexes. In this model, the transcription-repair coupling factor Cockayne Syndrome B (or the yeast equivalent Rad26) uses DNA translocase activity to remodel the Pol II-DNA interface, possibly to push the polymerase past the obstruction or to remove it from the DNA so that repair can take place if the obstacle is a DNA lesion. However, when this action is not possible and Pol II is left irreversibly trapped on DNA, the polymerase is instead ubiquitylated and eventually removed by proteolysis.

Key words: Transcription-coupled repair, Transcript elongation, Cockayne syndrome, Swi/Snf, Def1, Ubiquitylation, RNA polymerase II

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