ELL, a novel TFIIH partner, is involved in transcription restart after DNA repair

Autor: 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
Přispěvatelé: Institut de pharmacologie et de biologie structurale (IPBS), Université Toulouse III - Paul Sabatier (UT3), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-Centre National de la Recherche Scientifique (CNRS), Institut de Génétique et de Biologie Moléculaire et Cellulaire (IGBMC), Université de Strasbourg (UNISTRA)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Erasmus University Medical Center [Rotterdam] (Erasmus MC), Coin, Frédéric, Laboratoire de Physique Corpusculaire - Clermont-Ferrand (LPC), Université Blaise Pascal - Clermont-Ferrand 2 (UBP)-Institut National de Physique Nucléaire et de Physique des Particules du CNRS (IN2P3)-Centre National de la Recherche Scientifique (CNRS), CHU Dijon, Centre Hospitalier Universitaire de Dijon - Hôpital François Mitterrand (CHU Dijon), Centre National de la Recherche Scientifique (CNRS)-Université Toulouse III - Paul Sabatier (UT3), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées, Biochemistry, Molecular Genetics
Jazyk: angličtina
Rok vydání: 2013
Předmět:
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
Zdroj: 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
ISSN: 0027-8424
1091-6490
DOI: 10.1073/pnas.1305009110⟩
Popis: 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.
Databáze: OpenAIRE