期刊
JOURNAL OF MOLECULAR BIOLOGY
卷 382, 期 2, 页码 266-274出版社
ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
DOI: 10.1016/j.jmb.2008.07.018
关键词
Cockayne syndrome; CSB; RNA polymerase I; transcription initiation; elongation
资金
- German Research Foundation (Deutsche Forschungsgemeinschaft) [1B83 2-1 (KFO142)]
Mutations in the Cockayne syndrome B (CSB) gene result in the human form of Cockayne syndrome. CSB protein has been shown to be a component of RNA polymerase I (Pol I) transcription. In this study, we have analyzed at which step of the transcription cycle CSB influences in vitro transcription by RNA Pol I in an ATP-independent manner. Moreover, CSB can be cross-linked to the rDNA promoter and gene-internal sequences. Partial deletion mutants of CSB strongly repress Pol I in vitro transcription, indicating an inhibitory function of truncated CSB. In addition, evidence that mutant CSB inhibits the elongation step of Pol I transcription is presented. Lack of CSB expression does not impair Pol I transcription, showing that CSB is not essential for ribosomal transcription. Our results implicate that repressed Pol I transcription could be one factor contributing to the Cockayne syndrome phenotype. (C) 2008 Elsevier Ltd. All rights reserved.
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