Article
- The EMBO Journal (2006) 25, 1915 - 1923
- doi:10.1038/sj.emboj.7601071
Published online: 6 April 2006
Subject Categories:
Cockayne syndrome B protein regulates the transcriptional program after UV irradiation
Luca Proietti-De-Santis, Pascal Drané and Jean-Marc Egly
- Institut de Génétique et de Biologie Moléculaire et Cellulaire, CNRS/INSERM, Illkirch Cedex, CU Strasbourg, France
Correspondence to:
Jean-Marc Egly, Institut de Génétique et de Biologie Moléculaire et Cellulaire, CNRS/INSERM, BP 163, Illkirch Cedex, CU Strasbourg 67404, France. Tel.: +33 388 65 34 47; Fax: +33 388 65 32 01; E-mail: egly@igbmc.u-strasbg.fr
Received 3 February 2006; Accepted 7 March 2006
Abstract
The phenotype of the human genetic disorder Cockayne syndrome (CS) is not only due to DNA repair defect but also (and perhaps essentially) to a severe transcription initiation defect. After UV irradiation, even undamaged genes are not transcribed in CSB cells. Indeed, neither RNA pol II nor the associated basal transcription factors are recruited to the promoters of the housekeeping genes, around of which histone H4 acetylation is also deficient. Transfection of CSB restores the recruitment process of RNA pol II. On the contrary, the p53-responsive genes do not require CSB and are transcribed in both wild-type and CSB cells upon DNA damage. Altogether, our data highlight the pivotal role of CSB in initiating the transcriptional program of certain genes after UV irradiation, and also may explain some of the complex traits of CS patients.
Keywords:
- CSB,
- p53,
- RNA polymerase II,
- transcription initiation
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