The Cockayne syndrome B (CSB) protein is essential for transcription-coupled DNA repair (TCR), which is dependent on RNA polymerase II elongation. TCR is required to quickly remove the cytotoxic transcription-blocking DNA lesions. Functional GFP-tagged CSB, expressed at physiological levels, was homogeneously dispersed throughout the nucleoplasm in addition to bright nuclear foci and nucleolar accumulation. Photobleaching studies showed that GFP-CSB, as part of a high molecular weight complex, transiently interacts with the transcription machinery. Upon (DNA damage-induced) transcription arrest CSB binding these interactions are prolonged, most likely reflecting actual engagement of CSB in TCR. These findings are consistent with a model in which CSB monitors progression of transcription by regularly probing elongation complexes and becomes more tightly associated to these complexes when TCR is active.

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doi.org/10.1083/jcb.200401056, hdl.handle.net/1765/3218
The Journal of Cell Biology
Erasmus MC: University Medical Center Rotterdam

van den Boom, V, Citterio, E, Hoogstraten, D, Zotter, A, van Cappellen, W.A, Hoeijmakers, J.H.J, … Vermeulen, W. (2004). DNA damage stabilizes interaction of CSB with the transcription elongation machinery. The Journal of Cell Biology, 166(1), 27–36. doi:10.1083/jcb.200401056