A Ubiquitin-Binding Domain in Cockayne Syndrome B Required for Transcription-Coupled Nucleotide Excision Repair

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Standard

A Ubiquitin-Binding Domain in Cockayne Syndrome B Required for Transcription-Coupled Nucleotide Excision Repair. / Anindya, Roy; Mari, Pierre Olivier; Kristensen, Ulrik; Kool, Hanneke; Giglia-Mari, Giuseppina; Mullenders, Leon H.; Fousteri, Maria; Vermeulen, Wim; Egly, Jean Marc; Svejstrup, Jesper Q.

I: Molecular Cell, Bind 38, Nr. 5, 2010, s. 637-648.

Publikation: Bidrag til tidsskrift › Tidsskriftartikel › Forskning › fagfællebedømt

Harvard

Anindya, R, Mari, PO, Kristensen, U, Kool, H, Giglia-Mari, G, Mullenders, LH, Fousteri, M, Vermeulen, W, Egly, JM & Svejstrup, JQ 2010, 'A Ubiquitin-Binding Domain in Cockayne Syndrome B Required for Transcription-Coupled Nucleotide Excision Repair', Molecular Cell, bind 38, nr. 5, s. 637-648. https://doi.org/10.1016/j.molcel.2010.04.017

APA

Anindya, R., Mari, P. O., Kristensen, U., Kool, H., Giglia-Mari, G., Mullenders, L. H., Fousteri, M., Vermeulen, W., Egly, J. M., & Svejstrup, J. Q. (2010). A Ubiquitin-Binding Domain in Cockayne Syndrome B Required for Transcription-Coupled Nucleotide Excision Repair. Molecular Cell, 38(5), 637-648. https://doi.org/10.1016/j.molcel.2010.04.017

Vancouver

Anindya R, Mari PO, Kristensen U, Kool H, Giglia-Mari G, Mullenders LH o.a. A Ubiquitin-Binding Domain in Cockayne Syndrome B Required for Transcription-Coupled Nucleotide Excision Repair. Molecular Cell. 2010;38(5):637-648. https://doi.org/10.1016/j.molcel.2010.04.017

Author

Anindya, Roy ; Mari, Pierre Olivier ; Kristensen, Ulrik ; Kool, Hanneke ; Giglia-Mari, Giuseppina ; Mullenders, Leon H. ; Fousteri, Maria ; Vermeulen, Wim ; Egly, Jean Marc ; Svejstrup, Jesper Q. / A Ubiquitin-Binding Domain in Cockayne Syndrome B Required for Transcription-Coupled Nucleotide Excision Repair. I: Molecular Cell. 2010 ; Bind 38, Nr. 5. s. 637-648.

Bibtex

@article{55fdb90a2d7243e58d875f72afadac86,
title = "A Ubiquitin-Binding Domain in Cockayne Syndrome B Required for Transcription-Coupled Nucleotide Excision Repair",
abstract = "Transcription-coupled nucleotide excision repair (TC-NER) allows RNA polymerase II (RNAPII)-blocking lesions to be rapidly removed from the transcribed strand of active genes. Defective TCR in humans is associated with Cockayne syndrome (CS), typically caused by defects in either CSA or CSB. Here, we show that CSB contains a ubiquitin-binding domain (UBD). Cells expressing UBD-less CSB (CSBdel) have phenotypes similar to those of cells lacking CSB, but these can be suppressed by appending a heterologous UBD, so ubiquitin binding is essential for CSB function. Surprisingly, CSBdel remains capable of assembling nucleotide excision repair factors and repair synthesis proteins around damage-stalled RNAPII, but such repair complexes fail to excise the lesion. Together, our results indicate an essential role for protein ubiquitylation and CSB's UBD in triggering damage incision during TC-NER and allow us to integrate the function of CSA and CSB in a model for the process.",
keywords = "DNA, PROTEINS",
author = "Roy Anindya and Mari, {Pierre Olivier} and Ulrik Kristensen and Hanneke Kool and Giuseppina Giglia-Mari and Mullenders, {Leon H.} and Maria Fousteri and Wim Vermeulen and Egly, {Jean Marc} and Svejstrup, {Jesper Q.}",
note = "Funding Information: This work was supported by a grant from Cancer Research UK (to J.Q.S.). Work in the Svejstrup, Mullender, Vermeulen, and Egly laboratories was supported by a grant from the European Community (Integrated Project DNA repair, grant no. LSHG-CT-2005-512113). P.-O.M. and G.G.-M. were funded by the Association for International Cancer Research (AICR 07-0129), a “Young Researcher Program” ATIP(CNRS)/InCa (France), and Association pour la Recherche contre le Cancer (ARC, France) (contract for equipment n: 8505). We thank Dr Camille Godon for the technical assistance, Dr. Dominik Boos for suggestions, and Svejstrup lab members for helpful discussions. ",
year = "2010",
doi = "10.1016/j.molcel.2010.04.017",
language = "English",
volume = "38",
pages = "637--648",
journal = "Molecular Cell",
issn = "1097-2765",
publisher = "Cell Press",
number = "5",

}

RIS

TY - JOUR

T1 - A Ubiquitin-Binding Domain in Cockayne Syndrome B Required for Transcription-Coupled Nucleotide Excision Repair

AU - Anindya, Roy

AU - Mari, Pierre Olivier

AU - Kristensen, Ulrik

AU - Kool, Hanneke

AU - Giglia-Mari, Giuseppina

AU - Mullenders, Leon H.

AU - Fousteri, Maria

AU - Vermeulen, Wim

AU - Egly, Jean Marc

AU - Svejstrup, Jesper Q.

N1 - Funding Information: This work was supported by a grant from Cancer Research UK (to J.Q.S.). Work in the Svejstrup, Mullender, Vermeulen, and Egly laboratories was supported by a grant from the European Community (Integrated Project DNA repair, grant no. LSHG-CT-2005-512113). P.-O.M. and G.G.-M. were funded by the Association for International Cancer Research (AICR 07-0129), a “Young Researcher Program” ATIP(CNRS)/InCa (France), and Association pour la Recherche contre le Cancer (ARC, France) (contract for equipment n: 8505). We thank Dr Camille Godon for the technical assistance, Dr. Dominik Boos for suggestions, and Svejstrup lab members for helpful discussions.

PY - 2010

Y1 - 2010

N2 - Transcription-coupled nucleotide excision repair (TC-NER) allows RNA polymerase II (RNAPII)-blocking lesions to be rapidly removed from the transcribed strand of active genes. Defective TCR in humans is associated with Cockayne syndrome (CS), typically caused by defects in either CSA or CSB. Here, we show that CSB contains a ubiquitin-binding domain (UBD). Cells expressing UBD-less CSB (CSBdel) have phenotypes similar to those of cells lacking CSB, but these can be suppressed by appending a heterologous UBD, so ubiquitin binding is essential for CSB function. Surprisingly, CSBdel remains capable of assembling nucleotide excision repair factors and repair synthesis proteins around damage-stalled RNAPII, but such repair complexes fail to excise the lesion. Together, our results indicate an essential role for protein ubiquitylation and CSB's UBD in triggering damage incision during TC-NER and allow us to integrate the function of CSA and CSB in a model for the process.

AB - Transcription-coupled nucleotide excision repair (TC-NER) allows RNA polymerase II (RNAPII)-blocking lesions to be rapidly removed from the transcribed strand of active genes. Defective TCR in humans is associated with Cockayne syndrome (CS), typically caused by defects in either CSA or CSB. Here, we show that CSB contains a ubiquitin-binding domain (UBD). Cells expressing UBD-less CSB (CSBdel) have phenotypes similar to those of cells lacking CSB, but these can be suppressed by appending a heterologous UBD, so ubiquitin binding is essential for CSB function. Surprisingly, CSBdel remains capable of assembling nucleotide excision repair factors and repair synthesis proteins around damage-stalled RNAPII, but such repair complexes fail to excise the lesion. Together, our results indicate an essential role for protein ubiquitylation and CSB's UBD in triggering damage incision during TC-NER and allow us to integrate the function of CSA and CSB in a model for the process.

KW - DNA

KW - PROTEINS

U2 - 10.1016/j.molcel.2010.04.017

DO - 10.1016/j.molcel.2010.04.017

M3 - Journal article

C2 - 20541997

AN - SCOPUS:77953091336

VL - 38

SP - 637

EP - 648

JO - Molecular Cell

JF - Molecular Cell

SN - 1097-2765

IS - 5

ER -

ID: 330899519