Cited by 163DNA Repair MechanismsGenomics and Chromatin DynamicsNuclear Structure and Function

Cockayne syndrome B protein regulates the transcriptional program after UV irradiation

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Proietti‐De‐Santis, Luca, Drané, Pascal, Egly, Jean‐Marc·2006·The EMBO Journal

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.

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Crossref · 10.1038/sj.emboj.7601071

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  • Proietti-De-Santis et al. showed that CSB is required during the first phases of RNA polymerase II transcription initiation in living human cells.

    “In living human cells, Proietti-De-Santis et al. [225] have shown that CSB is required during the first phases of RNA pol II transcription initiation.”

    From Molecular Mechanisms of Ultraviolet Radiation‐Induced DNA Damage and Repair (2010) · cites this paper as [225]

    In “CSB is required for transcription initiation after UV irradiation,” the paper reports impaired initiation-complex formation and RNA polymerase II recruitment at certain promoters in UV-irradiated CSB cells. The citing sentence omits that UV-irradiation condition and generalizes the requirement: “CSB does not participate in p53-responsive gene expression” says those genes can be transcribed without CSB. Page numbers were not provided in our copy. (LLM, conf=0.87)

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Authors
Proietti‐De‐Santis, L., Drané, P., & Egly, J.
Affiliations
Centre National de la Recherche Scientifique (FR)
Corresponding author
Egly, Jean‐Marc
Venue
The EMBO Journal
Published
2006-04-06
Volume
25
Issue
9
Pages
1915-1923
ISSN
  • 0261-4189 (ISSN-L)
  • 1460-2075
OpenAlex
W2070933029
Cited by
163
References
33
Citations by year
2026: 3 · 2025: 7 · 2024: 9 · 2023: 4 · 2022: 7 · 2021: 11 · 2020: 6 · 2019: 5 · 2018: 9 · 2017: 9 · 2016: 5 · 2015: 3 · 2014: 9 · 2013: 18 · 2012: 14
FWCI
3.40
Type
journal article
Language
en
Open access
Locations
  • The EMBO Journal (publishedVersion)
  • Europe PMC (PubMed Central) (publishedVersion)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
  • HAL (submittedVersion)
Funders
  • Institut National de la Santé et de la Recherche Médicale
  • Fondation pour la Recherche Médicale
  • Ligue Contre le Cancer
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › DNA Repair Mechanisms
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Genomics and Chromatin Dynamics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Nuclear Structure and Function
Keywords
Cockayne syndrome, UV irradiation, transcription initiation, RNA polymerase II recruitment, histone H4 acetylation, DNA damage response, transcriptional programs, DNA repair deficiency
MeSH terms
Poly-ADP-Ribose Binding Proteins, Cockayne Syndrome, DNA, DNA Damage, DNA Repair, DNA Helicases, Gene Expression Regulation, Humans, Promoter Regions, Genetic, RNA Polymerase II, Tetrahydrofolate Dehydrogenase, Transcription, Genetic, Ultraviolet Rays, Tumor Suppressor Protein p53, Receptors, Calcitriol, DNA Repair Enzymes

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