Transcription-Coupled Nucleotide Excision Repair and the Transcriptional Response to UV-Induced DNA Damage
Publikation: Bidrag til tidsskrift › Review › Forskning › fagfællebedømt
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Transcription-Coupled Nucleotide Excision Repair and the Transcriptional Response to UV-Induced DNA Damage. / Nieto Moreno, Nicolás; Olthof, Anouk M.; Svejstrup, Jesper Q.
I: Annual Review of Biochemistry, Bind 92, 2023, s. 81-113.Publikation: Bidrag til tidsskrift › Review › Forskning › fagfællebedømt
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TY - JOUR
T1 - Transcription-Coupled Nucleotide Excision Repair and the Transcriptional Response to UV-Induced DNA Damage
AU - Nieto Moreno, Nicolás
AU - Olthof, Anouk M.
AU - Svejstrup, Jesper Q.
N1 - Publisher Copyright: Copyright © 2023 by the author(s).
PY - 2023
Y1 - 2023
N2 - Ultraviolet (UV) irradiation and other genotoxic stresses induce bulky DNA lesions, which threaten genome stability and cell viability. Cells have evolved two main repair pathways to remove such lesions: global genome nucleotide excision repair (GG-NER) and transcription-coupled nucleotide excision repair (TC-NER). The modes by which these subpathways recognize DNA lesions are distinct, but they converge onto the same downstream steps for DNA repair. Here, we first summarize the current understanding of these repair mechanisms, specifically focusing on the roles of stalled RNA polymerase II, Cockayne syndrome protein B (CSB), CSA and UV-stimulated scaffold protein A (UVSSA) in TC-NER. We also discuss the intriguing role of protein ubiquitylation in this process. Additionally, we highlight key aspects of the effect of UV irradiation on transcription and describe the role of signaling cascades in orchestrating this response. Finally, we describe the pathogenic mechanisms underlying xeroderma pigmentosum and Cockayne syndrome, the two main diseases linked to mutations in NER factors.
AB - Ultraviolet (UV) irradiation and other genotoxic stresses induce bulky DNA lesions, which threaten genome stability and cell viability. Cells have evolved two main repair pathways to remove such lesions: global genome nucleotide excision repair (GG-NER) and transcription-coupled nucleotide excision repair (TC-NER). The modes by which these subpathways recognize DNA lesions are distinct, but they converge onto the same downstream steps for DNA repair. Here, we first summarize the current understanding of these repair mechanisms, specifically focusing on the roles of stalled RNA polymerase II, Cockayne syndrome protein B (CSB), CSA and UV-stimulated scaffold protein A (UVSSA) in TC-NER. We also discuss the intriguing role of protein ubiquitylation in this process. Additionally, we highlight key aspects of the effect of UV irradiation on transcription and describe the role of signaling cascades in orchestrating this response. Finally, we describe the pathogenic mechanisms underlying xeroderma pigmentosum and Cockayne syndrome, the two main diseases linked to mutations in NER factors.
KW - Cockayne syndrome
KW - DNA repair
KW - global genome nucleotide excision repair
KW - RNA polymerase II
KW - transcription
KW - transcription-coupled nucleotide excision repair
U2 - 10.1146/annurev-biochem-052621-091205
DO - 10.1146/annurev-biochem-052621-091205
M3 - Review
C2 - 37040775
AN - SCOPUS:85163920851
VL - 92
SP - 81
EP - 113
JO - Annual Review of Biochemistry
JF - Annual Review of Biochemistry
SN - 0066-4154
ER -
ID: 362336928