ELL, a novel TFIIH partner, is involved in transcription restart after DNA repair
- Resource Type
- Authors
- Pierre-Olivier Mari; Christine Bordier; Anne Gonzales de Peredo; Anna Lagarou; Wim Vermeulen; Bernard Monsarrat; Lara Kaddoum; Joris Slingerland; Giuseppina Giglia-Mari; Violette Gautier; Sophie Mourgues; Amandine Mourcet; Frédéric Coin
- Source
- Proceedings of the National Academy of Sciences of the United States of America
Proceedings of the National Academy of Sciences of the United States of America, 2013, 110 (44), pp.17927-17932. ⟨10.1073/pnas.1305009110⟩
Proceedings of the National Academy of Sciences of the United States of America, National Academy of Sciences, 2013, 110 (44), pp.17927-17932. ⟨10.1073/pnas.1305009110⟩
Proceedings of the National Academy of Sciences of the U.S.A., 110(44), 17927-17932. National Academy of Sciences
- Subject
- Transcriptional Activation
Chromatin Immunoprecipitation
DNA Repair
[SDV]Life Sciences [q-bio]
Blotting, Western
Molecular Sequence Data
RNA polymerase II
Real-Time Polymerase Chain Reaction
Mass Spectrometry
Cell Line
03 medical and health sciences
0302 clinical medicine
Humans
Cloning, Molecular
Cockayne syndrome
RNA polymerase II holoenzyme
ComputingMilieux_MISCELLANEOUS
030304 developmental biology
DNA Primers
Genetics
CAK
0303 health sciences
Multidisciplinary
biology
General transcription factor
Base Sequence
LEC
[SDV.BBM.BM]Life Sciences [q-bio]/Biochemistry, Molecular Biology/Molecular biology
Sequence Analysis, DNA
Biological Sciences
elongation factor
[SDV] Life Sciences [q-bio]
030220 oncology & carcinogenesis
Transcription factor II H
biology.protein
Transcription factor II F
RNA Interference
RNA Polymerase II
Transcription factor II D
Transcriptional Elongation Factors
Transcription Factor TFIIH
Transcription factor II A
TCR
Nucleotide excision repair
Fluorescence Recovery After Photobleaching
- Language
- English
- ISSN
- 0027-8424
1091-6490
International audience; DNA lesions that block transcription may cause cell death even when repaired, if transcription does not restart to reestablish cellular metabolism. However, transcription resumption after individual DNA-lesion repair remains poorly described in mechanistic terms and its players are largely unknown. The general transcription factor II H (TFIIH) is a major actor of both nucleotide excision repair subpathways of which transcription-coupled repair highlights the interplay between DNA repair and transcription. Using an unbiased proteomic approach, we have identified the protein eleven-nineteen lysine-rich leukemia (ELL) as a TFIIH partner. Here we show that ELL is recruited to UV-damaged chromatin in a Cdk7- dependent manner (a component of the cyclin-dependent activating kinase subcomplex of TFIIH). We demonstrate that depletion of ELL strongly hinders RNA polymerase II (RNA Pol II) transcription resumption after lesion removal and DNA gap filling. Lack of ELL was also observed to increase RNA Pol II retention to the chromatin during this process. Identifying ELL as an essential player for RNA Pol II restart during cellular DNA damage response opens the way to obtaining a mechanistic description of transcription resumption after DNA repair.