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van den Boom, V. et al.

DNA damage stabilizes interaction of CSB with the transcription elongation machinery.

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.[1]

References

DNA damage stabilizes interaction of CSB with the transcription elongation machinery. van den Boom, V., Citterio, E., Hoogstraten, D., Zotter, A., Egly, J.M., van Cappellen, W.A., Hoeijmakers, J.H., Houtsmuller, A.B., Vermeulen, W. J. Cell Biol. (2004) [Pubmed]

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