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Cockayne syndrome B protein regulates the transcriptional program after UV irradiation
Author(s) -
ProiettiDeSantis Luca,
Drané Pascal,
Egly JeanMarc
Publication year - 2006
Publication title -
the embo journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 7.484
H-Index - 392
eISSN - 1460-2075
pISSN - 0261-4189
DOI - 10.1038/sj.emboj.7601071
Subject(s) - biology , cockayne syndrome , transcription (linguistics) , housekeeping gene , gene , dna repair , histone , genetics , dna damage , transcriptional regulation , rna polymerase ii , microbiology and biotechnology , epigenetics , dna , rna , acetylation , promoter , nucleotide excision repair , gene expression , linguistics , philosophy
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.