scholarly journals Rad26, the Transcription-Coupled Repair Factor in Yeast, Is Required for Removal of Stalled RNA Polymerase-II following UV Irradiation

PLoS ONE ◽  
2013 ◽  
Vol 8 (8) ◽  
pp. e72090 ◽  
Author(s):  
Sounak Ghosh-Roy ◽  
Dhiman Das ◽  
Debarati Chowdhury ◽  
Michael J.Smerdon ◽  
Ronita Nag Chaudhuri
Keyword(s):  
Rna Polymerase ◽  
Rna Polymerase Ii ◽  
Uv Irradiation ◽  
Repair Factor ◽  
Transcription Coupled Repair

scholarly journals CSB-Dependent Cyclin-Dependent Kinase 9 Degradation and RNA Polymerase II Phosphorylation during Transcription-Coupled Repair

2019 ◽  
Vol 39 (6) ◽  
Author(s):  
Lise-Marie Donnio ◽  
Anna Lagarou ◽  
Gabrielle Sueur ◽  
Pierre-Olivier Mari ◽  
Giuseppina Giglia-Mari
Keyword(s):  
Dna Repair ◽  
Rna Polymerase ◽  
Rna Polymerase Ii ◽  
Uv Irradiation ◽  
Dna Lesions ◽  
Premature Aging ◽  
Cyclin Dependent Kinase ◽  
Cyclin T1 ◽  
Group B ◽  
Transcription Coupled Repair

ABSTRACT DNA lesions block cellular processes such as transcription, inducing apoptosis, tissue failures, and premature aging. To counteract the deleterious effects of DNA damage, cells are equipped with various DNA repair pathways. Transcription-coupled repair specifically removes helix-distorting DNA adducts in a coordinated multistep process. This process has been extensively studied; however, once the repair reaction is accomplished, little is known about how transcription restarts. In this study, we show that, after UV irradiation, the cyclin-dependent kinase 9 (CDK9)/cyclin T1 kinase unit is specifically released from the HEXIM1 complex and that this released fraction is degraded in the absence of the Cockayne syndrome group B protein (CSB). We determine that UV irradiation induces a specific Ser2 phosphorylation of the RNA polymerase II and that this phosphorylation is CSB dependent. Surprisingly, CDK9 is not responsible for this phosphorylation but instead might play a nonenzymatic role in transcription restart after DNA repair.

scholarly journals Rad26p, a transcription-coupled repair factor, is recruited to the site of DNA lesion in an elongating RNA polymerase II-dependent manner in vivo

2009 ◽  
Vol 38 (5) ◽  
pp. 1461-1477 ◽  
Author(s):  
Shivani Malik ◽  
Priyasri Chaurasia ◽  
Shweta Lahudkar ◽  
Geetha Durairaj ◽  
Abhijit Shukla ◽  
...  
Keyword(s):  
Rna Polymerase ◽  
Rna Polymerase Ii ◽  
Dependent Manner ◽  
Dna Lesion ◽  
Repair Factor ◽  
Transcription Coupled Repair

scholarly journals CSB-dependent CDK9 degradation and RNA Polymerase II phosphorylation during Transcription Coupled Repair

2018 ◽  
Author(s):  
Lise-Marie Donnio ◽  
Anna Lagarou ◽  
Gabrielle Sueur ◽  
Pierre-Olivier Mari ◽  
Giuseppina Giglia-Mari
Keyword(s):  
Dna Repair ◽  
Rna Polymerase ◽  
Rna Polymerase Ii ◽  
Uv Irradiation ◽  
Dna Adducts ◽  
Dna Lesions ◽  
Step Process ◽  
Cellular Processes ◽  
Repair Pathways ◽  
Transcription Coupled Repair

AUTHOR SUMMARYDNA lesions block cellular processes such as transcription, inducing apoptosis, tissue failures and premature ageing. To counteract the deleterious effects of DNA damage, cells are equipped with various DNA repair pathways. Transcription Coupled Repair specifically removes helix-distorting DNA adducts in a coordinated multi-step process. This process has been extensively studied, however once the repair reaction is accomplished, little is known about how transcription restarts. In this study, we show that, after UV irradiation, the CDK9/CyclinT1 kinase unit is specifically released from the HEXIM1 complex and that this released fraction is degraded in the absence of CSB. We determine that UV-irradiation induces a specific Ser2 phosphorylation of the RNA polymerase II and that this phosphorylation is CSB dependent. Surprisingly CDK9 is not responsible for this phosphorylation but instead plays a non-enzymatic role in transcription restart after DNA repair.

scholarly journals Recognition of RNA Polymerase II and Transcription Bubbles by XPG, CSB, and TFIIH: Insights for Transcription-Coupled Repair and Cockayne Syndrome

2005 ◽  
Vol 20 (2) ◽  
pp. 187-198 ◽  
Author(s):  
Altaf H. Sarker ◽  
Susan E. Tsutakawa ◽  
Seth Kostek ◽  
Cliff Ng ◽  
David S. Shin ◽  
...  
Keyword(s):  
Rna Polymerase ◽  
Rna Polymerase Ii ◽  
Cockayne Syndrome ◽  
Transcription Coupled Repair

scholarly journals Mechanism of Rad26-assisted rescue of stalled RNA polymerase II in transcription-coupled repair

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Chunli Yan ◽  
Thomas Dodd ◽  
Jina Yu ◽  
Bernice Leung ◽  
Jun Xu ◽  
...  
Keyword(s):  
Rna Polymerase ◽  
Rna Polymerase Ii ◽  
Bound States ◽  
Dna Lesions ◽  
Functional Interpretation ◽  
Structural Mechanism ◽  
Disease Mutations ◽  
Dynamic Communities ◽  
Allosteric Pathway ◽  
Transcription Coupled Repair

AbstractTranscription-coupled repair is essential for the removal of DNA lesions from the transcribed genome. The pathway is initiated by CSB protein binding to stalled RNA polymerase II. Mutations impairing CSB function cause severe genetic disease. Yet, the ATP-dependent mechanism by which CSB powers RNA polymerase to bypass certain lesions while triggering excision of others is incompletely understood. Here we build structural models of RNA polymerase II bound to the yeast CSB ortholog Rad26 in nucleotide-free and bound states. This enables simulations and graph-theoretical analyses to define partitioning of this complex into dynamic communities and delineate how its structural elements function together to remodel DNA. We identify an allosteric pathway coupling motions of the Rad26 ATPase modules to changes in RNA polymerase and DNA to unveil a structural mechanism for CSB-assisted progression past less bulky lesions. Our models allow functional interpretation of the effects of Cockayne syndrome disease mutations.

scholarly journals Mechanistic insights in transcription-coupled nucleotide excision repair of ribosomal DNA

2018 ◽  
Vol 115 (29) ◽  
pp. E6770-E6779 ◽  
Author(s):  
Laurianne Daniel ◽  
Elena Cerutti ◽  
Lise-Marie Donnio ◽  
Julie Nonnekens ◽  
Christophe Carrat ◽  
...  
Keyword(s):  
Rna Polymerase ◽  
Nucleotide Excision Repair ◽  
Uv Irradiation ◽  
Ribosomal Dna ◽  
Excision Repair ◽  
Rna Polymerase I ◽  
Nucleotide Excision ◽  
Polymerase I ◽  
Uv Lesions ◽  
Transcription Coupled Repair

Nucleotide excision repair (NER) guarantees genome integrity against UV light-induced DNA damage. After UV irradiation, cells have to cope with a general transcriptional block. To ensure UV lesions repair specifically on transcribed genes, NER is coupled with transcription in an extremely organized pathway known as transcription-coupled repair. In highly metabolic cells, more than 60% of total cellular transcription results from RNA polymerase I activity. Repair of the mammalian transcribed ribosomal DNA has been scarcely studied. UV lesions severely block RNA polymerase I activity and the full transcription-coupled repair machinery corrects damage on actively transcribed ribosomal DNAs. After UV irradiation, RNA polymerase I is more bound to the ribosomal DNA and both are displaced to the nucleolar periphery. Importantly, the reentry of RNA polymerase I and the ribosomal DNA is dependent on the presence of UV lesions on DNA and independent of transcription restart.

scholarly journals Functional TFIIH Is Required for UV-Induced Translocation of CSA to the Nuclear Matrix

2007 ◽  
Vol 27 (7) ◽  
pp. 2538-2547 ◽  
Author(s):  
Masafumi Saijo ◽  
Tamami Hirai ◽  
Akiko Ogawa ◽  
Aki Kobayashi ◽  
Shinya Kamiuchi ◽  
...  
Keyword(s):  
Rna Polymerase ◽  
Rna Polymerase Ii ◽  
Uv Irradiation ◽  
Nuclear Matrix ◽  
Mammalian Cells ◽  
Insoluble Fraction ◽  
Dnase I ◽  
Free System ◽  
Cell Free System ◽  
A Cell

ABSTRACT Transcription-coupled repair (TCR) efficiently removes a variety of lesions from the transcribed strand of active genes. Mutations in Cockayne syndrome group A and B genes (CSA and CSB) result in defective TCR, but the molecular mechanism of TCR in mammalian cells is not clear. We have found that CSA protein is translocated to the nuclear matrix after UV irradiation and colocalized with the hyperphosphorylated form of RNA polymerase II and that the translocation is dependent on CSB. We developed a cell-free system for the UV-induced translocation of CSA. A cytoskeleton (CSK) buffer-soluble fraction containing CSA and a CSK buffer-insoluble fraction prepared from UV-irradiated CS-A cells were mixed. After incubation, the insoluble fraction was treated with DNase I. CSA protein was detected in the DNase I-insoluble fraction, indicating that it was translocated to the nuclear matrix. In this cell-free system, the translocation was dependent on UV irradiation, CSB function, and TCR-competent CSA. Moreover, the translocation was dependent on functional TFIIH, as well as chromatin structure and transcription elongation. These results suggest that alterations of chromatin at the RNA polymerase II stall site, which depend on CSB and TFIIH at least, are necessary for the UV-induced translocation of CSA to the nuclear matrix.

scholarly journals ELOF1 is a transcription-coupled DNA repair factor that directs RNA polymerase II ubiquitylation

2021 ◽  
Author(s):  
Yana van der Weegen ◽  
Klaas de Lint ◽  
Diana van den Heuvel ◽  
Yuka Nakazawa ◽  
Tycho E. T. Mevissen ◽  
...  
Keyword(s):  
Dna Repair ◽  
Rna Polymerase ◽  
Rna Polymerase Ii ◽  
Repair Factor
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