Transcription-coupled repair and the transcriptional response to UV-Irradiation

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Transcription-coupled repair and the transcriptional response to UV-Irradiation. / Gaul, Liam; Svejstrup, Jesper Q.

In: DNA Repair, Vol. 107, 103208, 2021.

Research output: Contribution to journalJournal articleResearchpeer-review

Harvard

Gaul, L & Svejstrup, JQ 2021, 'Transcription-coupled repair and the transcriptional response to UV-Irradiation', DNA Repair, vol. 107, 103208. https://doi.org/10.1016/j.dnarep.2021.103208

APA

Gaul, L., & Svejstrup, J. Q. (2021). Transcription-coupled repair and the transcriptional response to UV-Irradiation. DNA Repair, 107, [103208]. https://doi.org/10.1016/j.dnarep.2021.103208

Vancouver

Gaul L, Svejstrup JQ. Transcription-coupled repair and the transcriptional response to UV-Irradiation. DNA Repair. 2021;107. 103208. https://doi.org/10.1016/j.dnarep.2021.103208

Author

Gaul, Liam ; Svejstrup, Jesper Q. / Transcription-coupled repair and the transcriptional response to UV-Irradiation. In: DNA Repair. 2021 ; Vol. 107.

Bibtex

@article{ddc054dff5bb44229e03443f1fb76366,
title = "Transcription-coupled repair and the transcriptional response to UV-Irradiation",
abstract = "Lesions in genes that result in RNA polymerase II (RNAPII) stalling or arrest are particularly toxic as they are a focal point of genome instability and potently block further transcription of the affected gene. Thus, cells have evolved the transcription-coupled nucleotide excision repair (TC-NER) pathway to identify damage-stalled RNAPIIs, so that the lesion can be rapidly repaired and transcription can continue. However, despite the identification of several factors required for TC-NER, how RNAPII is remodelled, modified, removed, or whether this is even necessary for repair remains enigmatic, and theories are intensely contested. Recent studies have further detailed the cellular response to UV-induced ubiquitylation and degradation of RNAPII and its consequences for transcription and repair. These advances make it pertinent to revisit the TC-NER process in general and with specific discussion of the fate of RNAPII stalled at DNA lesions.",
keywords = "Cockayne syndrome, Nucleotide excision repair, Transcription-coupled nucleotide excision repair, Ubiquitin, UVSSA, Xeroderma pigmentosum",
author = "Liam Gaul and Svejstrup, {Jesper Q.}",
note = "Publisher Copyright: {\textcopyright} 2021",
year = "2021",
doi = "10.1016/j.dnarep.2021.103208",
language = "English",
volume = "107",
journal = "DNA Repair",
issn = "1568-7864",
publisher = "Elsevier",

}

RIS

TY - JOUR

T1 - Transcription-coupled repair and the transcriptional response to UV-Irradiation

AU - Gaul, Liam

AU - Svejstrup, Jesper Q.

N1 - Publisher Copyright: © 2021

PY - 2021

Y1 - 2021

N2 - Lesions in genes that result in RNA polymerase II (RNAPII) stalling or arrest are particularly toxic as they are a focal point of genome instability and potently block further transcription of the affected gene. Thus, cells have evolved the transcription-coupled nucleotide excision repair (TC-NER) pathway to identify damage-stalled RNAPIIs, so that the lesion can be rapidly repaired and transcription can continue. However, despite the identification of several factors required for TC-NER, how RNAPII is remodelled, modified, removed, or whether this is even necessary for repair remains enigmatic, and theories are intensely contested. Recent studies have further detailed the cellular response to UV-induced ubiquitylation and degradation of RNAPII and its consequences for transcription and repair. These advances make it pertinent to revisit the TC-NER process in general and with specific discussion of the fate of RNAPII stalled at DNA lesions.

AB - Lesions in genes that result in RNA polymerase II (RNAPII) stalling or arrest are particularly toxic as they are a focal point of genome instability and potently block further transcription of the affected gene. Thus, cells have evolved the transcription-coupled nucleotide excision repair (TC-NER) pathway to identify damage-stalled RNAPIIs, so that the lesion can be rapidly repaired and transcription can continue. However, despite the identification of several factors required for TC-NER, how RNAPII is remodelled, modified, removed, or whether this is even necessary for repair remains enigmatic, and theories are intensely contested. Recent studies have further detailed the cellular response to UV-induced ubiquitylation and degradation of RNAPII and its consequences for transcription and repair. These advances make it pertinent to revisit the TC-NER process in general and with specific discussion of the fate of RNAPII stalled at DNA lesions.

KW - Cockayne syndrome

KW - Nucleotide excision repair

KW - Transcription-coupled nucleotide excision repair

KW - Ubiquitin

KW - UVSSA

KW - Xeroderma pigmentosum

U2 - 10.1016/j.dnarep.2021.103208

DO - 10.1016/j.dnarep.2021.103208

M3 - Journal article

C2 - 34416541

AN - SCOPUS:85112758735

VL - 107

JO - DNA Repair

JF - DNA Repair

SN - 1568-7864

M1 - 103208

ER -

ID: 276700034