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Cited by 103DNA Repair MechanismsDNA and Nucleic Acid ChemistryDiffusion and Search Dynamics

Recognition of nonhybridizing base pairs during nucleotide excision repair of DNA

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Buschta-Hedayat, Neda, Buterin, Tonko, Hess, Martin T., Missura, Miriam, Naegeli, Hanspeter·1999·Proceedings of the National Academy of Sciences
DOI 10.1073/pnas.96.11.6090PMC PMC26840
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Abstract

Nondistorting C4′ backbone adducts serve as molecular tools to analyze the strategy by which a limited number of human nucleotide excision repair (NER) factors recognize an infinite variety of DNA lesions. We have constructed composite DNA substrates containing a noncomplementary site adjacent to a nondistorting C4′ adduct to show that the loss of hydrogen bonding contacts between partner strands is an essential signal for the recruitment of NER enzymes. This specific conformational requirement for excision is mediated by the affinity of xeroderma pigmentosum group A (XPA) protein for nonhybridizing sites in duplex DNA. XPA recognizes defective Watson–Crick base pair conformations even in the absence of DNA adducts or other covalent modifications, apparently through detection of hydrophobic base components that are abnormally exposed to the double helical surface. This recognition function of XPA is enhanced by replication protein A (RPA) such that, in combination, XPA and RPA constitute a potent molecular sensor of denatured base pairs. Our results indicate that the XPA–RPA complex may promote damage recognition by monitoring Watson–Crick base pair integrity, thereby recruiting the human NER system preferentially to sites where hybridization between complementary strands is weakened or entirely disrupted.

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  • G4s and non-B DNA structures in general have been shown to trigger genomic instability through wrongfully stimulating DNA damage and repair responses which initially maintain genome integrity.

    “Notably, G4s and non-B DNA structures in general have been shown to trigger genomic instability through wrongfully stimulating DNA damage and repair responses which initially maintain genome integrity.”

    From G-quadruplex-mediated genomic instability drives SNVs in cancer (2024) · cites this paper as [81]

    The Results (page not available in our copy) show that nonhybridizing bases stimulate nucleotide excision repair when paired with a C4′ adduct, supporting the narrower point that altered base pairing can recruit a repair response. The paper does not examine G4s or non-B DNA structures generally, or show that inappropriate repair of those structures causes genomic instability; it reports that mismatched bases alone caused no excision. (LLM, conf=0.86)

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Cited by

Sorted by citations

Authors
Buschta-Hedayat, N., Buterin, T., Hess, M. T., Missura, M., & Naegeli, H.
Affiliations
University of Zurich (CH)
ORCID
Venue
Proceedings of the National Academy of Sciences
Publisher
National Academy of Sciences
Published
1999-05-25
Volume
96
Issue
11
Pages
6090-6095
ISSN
  • 0027-8424 (ISSN-L)
  • 1091-6490
DOI
10.1073/pnas.96.11.6090
PMC
PMC26840
OpenAlex
W1994982452
Cited by
103
References
3
Citations by year
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FWCI
2.65
Type
journal article
Language
en
Open access
Locations
  • Proceedings of the National Academy of Sciences (publishedVersion)
  • Europe PMC (PubMed Central) (publishedVersion)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › DNA Repair Mechanisms
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › DNA and Nucleic Acid Chemistry
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Diffusion and Search Dynamics
Keywords
nucleotide excision repair, XPA, replication protein A, DNA damage recognition, hydrogen bonding, DNA conformation, xeroderma pigmentosum
MeSH terms
Base Sequence, Binding Sites, DNA, DNA Repair, DNA-Binding Proteins, HeLa Cells, Humans, Nucleic Acid Conformation, Nucleic Acid Denaturation, Oligodeoxyribonucleotides, Substrate Specificity, Xeroderma Pigmentosum, Base Pairing, Replication Protein A, Xeroderma Pigmentosum Group A Protein

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