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 |
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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 |
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