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TRiC controls transcription resumption after UV damage by regulating Cockayne syndrome protein A
Transcription-blocking DNA lesions are removed by transcription-coupled nucleotide excision repair (TC-NER) to preserve cell viability. TC-NER is triggered by the stalling of RNA polymerase II at DNA lesions, leading to the recruitment of TC-NER-specific factors such as the CSA–DDB1–CUL4A–RBX1 culli...
Autores principales: | , , , , , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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Nature Publishing Group UK
2018
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5847541/ https://www.ncbi.nlm.nih.gov/pubmed/29531219 http://dx.doi.org/10.1038/s41467-018-03484-6 |
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author | Pines, Alex Dijk, Madelon Makowski, Matthew Meulenbroek, Elisabeth M. Vrouwe, Mischa G. van der Weegen, Yana Baltissen, Marijke French, Pim J. van Royen, Martin E. Luijsterburg, Martijn S. Mullenders, Leon H. Vermeulen, Michiel Vermeulen, Wim Pannu, Navraj S. van Attikum, Haico |
author_facet | Pines, Alex Dijk, Madelon Makowski, Matthew Meulenbroek, Elisabeth M. Vrouwe, Mischa G. van der Weegen, Yana Baltissen, Marijke French, Pim J. van Royen, Martin E. Luijsterburg, Martijn S. Mullenders, Leon H. Vermeulen, Michiel Vermeulen, Wim Pannu, Navraj S. van Attikum, Haico |
author_sort | Pines, Alex |
collection | PubMed |
description | Transcription-blocking DNA lesions are removed by transcription-coupled nucleotide excision repair (TC-NER) to preserve cell viability. TC-NER is triggered by the stalling of RNA polymerase II at DNA lesions, leading to the recruitment of TC-NER-specific factors such as the CSA–DDB1–CUL4A–RBX1 cullin–RING ubiquitin ligase complex (CRL(CSA)). Despite its vital role in TC-NER, little is known about the regulation of the CRL(CSA) complex during TC-NER. Using conventional and cross-linking immunoprecipitations coupled to mass spectrometry, we uncover a stable interaction between CSA and the TRiC chaperonin. TRiC’s binding to CSA ensures its stability and DDB1-dependent assembly into the CRL(CSA) complex. Consequently, loss of TRiC leads to mislocalization and depletion of CSA, as well as impaired transcription recovery following UV damage, suggesting defects in TC-NER. Furthermore, Cockayne syndrome (CS)-causing mutations in CSA lead to increased TRiC binding and a failure to compose the CRL(CSA) complex. Thus, we uncover CSA as a TRiC substrate and reveal that TRiC regulates CSA-dependent TC-NER and the development of CS. |
format | Online Article Text |
id | pubmed-5847541 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2018 |
publisher | Nature Publishing Group UK |
record_format | MEDLINE/PubMed |
spelling | pubmed-58475412018-03-15 TRiC controls transcription resumption after UV damage by regulating Cockayne syndrome protein A Pines, Alex Dijk, Madelon Makowski, Matthew Meulenbroek, Elisabeth M. Vrouwe, Mischa G. van der Weegen, Yana Baltissen, Marijke French, Pim J. van Royen, Martin E. Luijsterburg, Martijn S. Mullenders, Leon H. Vermeulen, Michiel Vermeulen, Wim Pannu, Navraj S. van Attikum, Haico Nat Commun Article Transcription-blocking DNA lesions are removed by transcription-coupled nucleotide excision repair (TC-NER) to preserve cell viability. TC-NER is triggered by the stalling of RNA polymerase II at DNA lesions, leading to the recruitment of TC-NER-specific factors such as the CSA–DDB1–CUL4A–RBX1 cullin–RING ubiquitin ligase complex (CRL(CSA)). Despite its vital role in TC-NER, little is known about the regulation of the CRL(CSA) complex during TC-NER. Using conventional and cross-linking immunoprecipitations coupled to mass spectrometry, we uncover a stable interaction between CSA and the TRiC chaperonin. TRiC’s binding to CSA ensures its stability and DDB1-dependent assembly into the CRL(CSA) complex. Consequently, loss of TRiC leads to mislocalization and depletion of CSA, as well as impaired transcription recovery following UV damage, suggesting defects in TC-NER. Furthermore, Cockayne syndrome (CS)-causing mutations in CSA lead to increased TRiC binding and a failure to compose the CRL(CSA) complex. Thus, we uncover CSA as a TRiC substrate and reveal that TRiC regulates CSA-dependent TC-NER and the development of CS. Nature Publishing Group UK 2018-03-12 /pmc/articles/PMC5847541/ /pubmed/29531219 http://dx.doi.org/10.1038/s41467-018-03484-6 Text en © The Author(s) 2018 Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/. |
spellingShingle | Article Pines, Alex Dijk, Madelon Makowski, Matthew Meulenbroek, Elisabeth M. Vrouwe, Mischa G. van der Weegen, Yana Baltissen, Marijke French, Pim J. van Royen, Martin E. Luijsterburg, Martijn S. Mullenders, Leon H. Vermeulen, Michiel Vermeulen, Wim Pannu, Navraj S. van Attikum, Haico TRiC controls transcription resumption after UV damage by regulating Cockayne syndrome protein A |
title | TRiC controls transcription resumption after UV damage by regulating Cockayne syndrome protein A |
title_full | TRiC controls transcription resumption after UV damage by regulating Cockayne syndrome protein A |
title_fullStr | TRiC controls transcription resumption after UV damage by regulating Cockayne syndrome protein A |
title_full_unstemmed | TRiC controls transcription resumption after UV damage by regulating Cockayne syndrome protein A |
title_short | TRiC controls transcription resumption after UV damage by regulating Cockayne syndrome protein A |
title_sort | tric controls transcription resumption after uv damage by regulating cockayne syndrome protein a |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5847541/ https://www.ncbi.nlm.nih.gov/pubmed/29531219 http://dx.doi.org/10.1038/s41467-018-03484-6 |
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