Cited by 65DNA Repair MechanismsNuclear Structure and FunctionBacterial Genetics and Biotechnology

Transcription-coupled repair: An update

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Spivak, Graciela·2016·Archives of Toxicology

Abstract

Nucleotide excision repair (NER) is a versatile pathway that removes helix-distorting DNA lesions from the genomes of organisms across the evolutionary scale, from bacteria to humans. The serial steps in NER involve recognition of lesions, adducts or structures that disrupt the DNA double helix, removal of a short oligonucleotide containing the offending lesion, synthesis of a repair patch copying the opposite undamaged strand, and ligation, to restore the DNA to its original form. Transcription-coupled repair (TCR) is a subpathway of NER dedicated to the repair of lesions that, by virtue of their location on the transcribed strands of active genes, encumber elongation by RNA polymerases. In this review, I report on recent findings that contribute to the elucidation of TCR mechanisms in the bacterium Escherichia coli, the yeast Saccharomyces cerevisiae and human cells. I review general models for the biochemical pathways and how and when cells might choose to utilize TCR or other pathways for repair or bypass of transcription-blocking DNA alterations.

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  • CSB may stimulate assembly of other components of TC-NER complex.

    “It may also stimulate the assembly of other components of TC-NER complex [98]”
  • Upon binding with RNAPII, CSB alters DNA conformation by wrapping DNA around the protein itself and changing association of RNAPII with DNA.

    “Upon binding with RNAPII, CSB alters the DNA conformation by wrapping the DNA around the protein itself and changing the association of RNAPII with DNA.”
  • The temporal hierarchy of NER of UV-induced dipyrimidine photoproducts in mammalian cells is characterized by rapid recognition and excision of 6-4 PPs and preferential repair of CPDs in actively transcribed genes.

    “The temporal hierarchy of NER of UV-induced dipyrimidine photoproducts in mammalian cells is characterized by not only rapid recognition and excision of 6–4 PPs (which are preferentially formed in open chromatin regions), but also preferential repair of CPDs in actively transcribed genes22–24.”

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Authors
Spivak, G.
Affiliations
Stanford University (US)
Corresponding author
Spivak, Graciela
Venue
Archives of Toxicology
Published
2016-08-22
Volume
90
Issue
11
Pages
2583-2594
ISSN
  • 0340-5761 (ISSN-L)
  • 1432-0738
OpenAlex
W2512730870
Cited by
65
References
91
Citations by year
2026: 5 · 2025: 1 · 2024: 1 · 2023: 4 · 2022: 8 · 2021: 6 · 2020: 7 · 2019: 8 · 2018: 12 · 2017: 13
FWCI
5.72
Type
journal article
Language
en
Open access
Locations
  • Archives of Toxicology (publishedVersion)
  • PubMed (publishedVersion)
  • PubMed Central (acceptedVersion)
Funders
National Institute of Environmental Health Sciences (5RO1 CA077712)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › DNA Repair Mechanisms
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Nuclear Structure and Function
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Bacterial Genetics and Biotechnology
Keywords
transcription-coupled repair, nucleotide excision repair, DNA damage recognition, RNA polymerase stalling, DNA repair pathways, Escherichia coli, Saccharomyces cerevisiae, human cells, repair pathway choice
MeSH terms
Animals, DNA Repair, Escherichia coli, Biological Evolution, Humans, Models, Biological, Mutagens, Saccharomyces cerevisiae, Species Specificity, Transcription, Genetic, Ultraviolet Rays, Gene Expression Regulation, Bacterial, Gene Expression Regulation, Developmental, Chromatin Assembly and Disassembly

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