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DNA damage stabilizes interaction of CSB with the transcription elongation machinery

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van den Boom, Vincent | Citterio, Elisabetta | Hoogstraten, Deborah | Zotter, Angelika | Egly, Jean-Marc | van Cappellen, Wiggert A. | Hoeijmakers, Jan H.J. | Houtsmuller, Adriaan B. | Vermeulen, Wim

Edité par CCSD ; Rockefeller University Press -

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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