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Cited by 71DNA Repair MechanismsCarcinogens and Genotoxicity AssessmentDNA and Nucleic Acid Chemistry

Gap-filling and bypass at the replication fork are both active mechanisms for tolerance of low-dose ultraviolet-induced DNA damage in the human genome

Open access
Quinet, Annabel, Vessoni, Alexandre T., Rocha, Clarissa R.R., Gottifredi, Vanesa, Biard, Denis, Sarasin, Alain, Menck, Carlos F.M., Stary, Anne·2014·DNA Repair
DOI 10.1016/j.dnarep.2013.12.005
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Abstract

Ultraviolet (UV)-induced DNA damage are removed by nucleotide excision repair (NER) or can be tolerated by specialized translesion synthesis (TLS) polymerases, such as Polη. TLS may act at stalled replication forks or through an S-phase independent gap-filling mechanism. After UVC irradiation, Polη-deficient (XP-V) human cells were arrested in early S-phase and exhibited both single-strand DNA (ssDNA) and prolonged replication fork stalling, as detected by DNA fiber assay. In contrast, NER deficiency in XP-C cells caused no apparent defect in S-phase progression despite the accumulation of ssDNA and a G2-phase arrest. These data indicate that while Polη is essential for DNA synthesis at ongoing damaged replication forks, NER deficiency might unmask the involvement of tolerance pathway through a gap-filling mechanism. ATR knock down by siRNA or caffeine addition provoked increased cell death in both XP-V and XP-C cells exposed to low-dose of UVC, underscoring the involvement of ATR/Chk1 pathway in both DNA damage tolerance mechanisms. We generated a unique human cell line deficient in XPC and Polη proteins, which exhibited both S- and G2-phase arrest after UVC irradiation, consistent with both single deficiencies. In these XP-C/Polη(KD) cells, UVC-induced replicative intermediates may collapse into double-strand breaks, leading to cell death. In conclusion, both TLS at stalled replication forks and gap-filling are active mechanisms for the tolerance of UVC-induced DNA damage in human cells and the preference for one or another pathway depends on the cellular genotype.

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Crossref · 10.1016/j.dnarep.2013.12.005

Cites

56 of 56 references verified0 citation errors · 0 not checkable

Statistics

Nothing to recompute.

Claims the paper makes

0 of 42 cited sources checked · 0 supported · 0 flagged

  • Findingown data

    XP-V cells accumulate single-stranded DNA after UVC irradiation.

    “exhibited both single-strand DNA (ssDNA) and prolonged replication fork stalling”
    • Also stated in: § 3.3. Persistent H2AX phosphorylation in XP-V, XP-C and XP-C/PolÁ KD human cells exposed to low-dose UVC · plain
      “deficient cell lines presented slightly more ssDNA than XP-C cor cells”
    Quote in the paperSubstantial claim
  • Findingown data

    XP-C cells accumulate in G2 phase after low-dose UVC.

    “a G2phase arrest”
    • Also stated in: § 3.1. XP-C human cells temporarily accumulate in G2-phase after low-dose UVC irradiation · plain
      “we detected a two-fold increase in the number of XP-C fibroblasts in G2-phase relative to control cells”
    Quote in the paperSubstantial claim
  • Findingown data

    ATR knockdown by siRNA or caffeine addition increases cell death in XP-V and XP-C cells exposed to low-dose UVC.

    “ATR knock down by siRNA or caffeine addition provoked increased cell death in both XP-V and XP-C cells exposed to low-dose of UVC”
    • Also stated in: § 3.6. Caffeine highly sensitizes GG-NER-deficient cells exposed to low-dose UVC irradiation · plain
      “CAF induced an increase in SubG1 cells in all irradiated deficient cell lines”
    Quote in the paperSubstantial claim
  • Findingown data

    XP-C/Polη KD cells exhibit both S- and G2-phase arrest after UVC irradiation.

    “We generated a unique human cell line deficient in XPC and Pol␩ proteins, which exhibited both S-and G2-phase arrest after UVC irradiation, consistent with both single deficiencies.”
    • Also stated in: § 3.2. Deficiency in both XPC and PolÁ proteins triggers accumulation in S-and G2-phases after low-dose UVC irradiation · plain
      “XP-C/Pol␩ KD fibroblasts accumulated in both G2and S-phases.”
    Quote in the paperSubstantial claim
  • Findingown data

    XP-C cells show no apparent defect in S-phase progression after UVC despite ssDNA accumulation and G2 arrest.

    “NER deficiency in XP-C cells caused no apparent defect in S-phase progression despite the accumulation of ssDNA and a G2phase arrest.”
    • Also stated in: § 3.1. XP-C human cells temporarily accumulate in G2-phase after low-dose UVC irradiation · plain
      “24 h after irradiation, DNA replication proceeded normally in XP-C cells, as evidenced by no decrease in either BrdU incorporation or cell accumulation in S-phase”
    Quote in the paperSubstantial claim
  • The quote only partly states this claim. 2
  • May combine two claims. 27
  • Classified as probably not a substantial claim. 13

  • The quote only partly states this claim.

    Findingown data

    XP-C cells accumulate ssDNA after UVC irradiation.

    “accumulation of ssDNA”
    • Also stated in: § 3.3. Persistent H2AX phosphorylation in XP-V, XP-C and XP-C/PolÁ KD human cells exposed to low-dose UVC · plain
      “deficient cell lines presented slightly more ssDNA than XP-C cor cells”
    Quote in the paperSubstantial claim

  • May combine two claims.

    Findingown data

    In deficient cell lines, γH2AX formation occurs in all cell cycle phases, with a more pronounced signal mainly in S-phase.

    “In all deficient cell lines, the formation of ␥H2AX was observed in all cell cycle phases, although the staining appeared in an arc-form, revealing a more pronounced signal mainly in S-phase.”
    Quote in the paperNot a substantial claim

  • May combine two claims.

    Findingown data

    At 24 hours after UVC, DNA replication proceeds normally in XP-C cells, with no decrease in BrdU incorporation or S-phase accumulation.

    “Interestingly, 24 h after irradiation, DNA replication proceeded normally in XP-C cells, as evidenced by no decrease in either BrdU incorporation or cell accumulation in S-phase (Fig. 1B).”
    Quote in the paperSubstantial claim

  • May combine two claims.

    Findingown data

    XP-C, XP-V, and XP-C/Polη KD fibroblasts show strongly decreased proliferation after combined UVC and caffeine treatment, whereas XP-C cor fibroblasts are not affected.

    “Although the proliferation of XP-C cor fibroblasts after UVC treatment was not affected by this drug, XP-C, XP-V and XP-C/Pol␩ KD fibroblasts displayed a strong decreased proliferation after combined UVC irradiation (2 and 3 J/m 2 ) and CAF treatment (Fig. 2B).”
    Quote in the paperSubstantial claim

  • May combine two claims.

    Findingown data

    A 2 J/m2 UVC dose does not induce detectable sensitivity in XP-C cor cells and causes only a mild effect on XP-C cells, with 70% proliferation compared to untreated XP-C cells.

    “First, we used a “low UVC dose” (2 J/m 2 ) that we defined as a UVC dose that does not induce any detectable sensitivity in XP-C cor cells and only a mild effect on XP-C cells (70% of cell proliferation compared to untreated XP-C cells, Fig. S2).”
    Quote in the paperSubstantial claim

  • May combine two claims.

    Findingown data

    At 24 hours after 2 J/m2 UVC, XP-C and XP-V cells accumulate in G2 and early S-phase respectively, while XP-C/Polη KD cells accumulate in both G2 and S phases.

    “At 24 h post 2 J/m 2 , while XP-C and XP-V cells accumulated in G2 and early S-phase, respectively (compare Figs. 1B and 2C), XP-C/Pol␩ KD fibroblasts accumulated in both G2and S-phases.”
    Quote in the paperSubstantial claim

  • May combine two claims.

    Findingown data

    No DNA strand breaks are detected immediately after UVC exposure, indicating that they are not directly induced by this irradiation.

    “Importantly, no DNA strand breaks were detected immediately after UVC exposure, indicating that they are not directly induced by this irradiation (Fig. S4).”
    Quote in the paperSubstantial claim

  • May combine two claims. The quote only partly states this claim.

    Findingown data

    In the absence of Polη, lesion bypass during S-phase is impaired, leading to prolonged S-phase arrest.

    “leading to a prolonged S-phase arrest in its absence”
    Quote in the paperSubstantial claim

  • May combine two claims.

    Findingown data

    More intense γH2AX staining is detected in S- and G2-phase XP-V and XP-C/Polη KD cells 24 hours after UVC, and is persistent and more pronounced in the double-deficient cell line.

    “a more intense ␥H2AX staining, distinguishable from the staining exhibited by the majority of cells, (see Fig. 3B, indicated as high levels of ␥H2AX), was detected in S-and G2-phase XP-V and XP-C/Pol␩ KD cells 24 h after UVC, which was persistent and much more pronounced in the double-deficient cell line.”
    Quote in the paperSubstantial claim

  • May combine two claims.

    Findingown data

    XP-C cells accumulate in G2-phase after 2 J/m2 and in late S- and G2-phases after 5 J/m2.

    “we noticed an accumulation of XP-C cells in G2phase after 2 J/m 2 and in late S-and G2-phases upon 5 J/m 2 (Fig. 1)”
    Quote in the paperSubstantial claim

  • May combine two claims.

    Findingown data

    At 72 hours, XP-C/Polη KD cells show a disrupted S-to-G2 transition and greater G2 accumulation (36%) than at 24 hours (24%).

    “At 72 h, BrdU incorporation assay showed a clear disrupted S-to G2-phase transition in XP-C/Pol␩ KD cells, and a greater accumulation of cells in G2-phase than that observed 24 h after UVC (36% compared to 24%).”
    Quote in the paperSubstantial claim

  • May combine two claims.

    Findingown data

    At 20 min after irradiation, XP-C cells show more pronounced replication fork stalling than XP-C cor cells, which is overcome at 60 min.

    “at 20 min after irradiation, XP-C cells exhibited a more pronounced replication fork stalling, compared to XP-C cor cells, that was overcome at 60 min time point (Fig. 5)”
    Quote in the paperSubstantial claim

  • May combine two claims.

    Findingown data

    XP-V cells contain single-strand breaks but not double-strand breaks after UVC.

    “we detected single-strand breaks (SSBs), but not DSBs, in XP-V cells (Fig. 4A and B)”
    Quote in the paperSubstantial claim

  • May combine two claims.

    Findingown data

    XP-C/Polη KD cells show irreversible cell cycle disruption, DSBs, and apoptosis induction after low UVC dose.

    “XP-C/Pol␩ KD cells showed an irreversible cell cycle disruption (Fig. 2C), DSBs (Fig. 4B) and apoptosis induction (Figs.2E and 6C) after a low UVC dose”
    Quote in the paperSubstantial claim

  • Classified as probably not a substantial claim. May combine two claims.

    Premisecitation

    UV light induces DNA damage that blocks replication and transcription, triggering either cell death or genetic instability.

    “Ultraviolet (UV) light induces DNA damage that blocks replication and transcription [1][2][3] triggering either cell death or genetic instability.”
    Quote in the paperSubstantial claim0 of 3 sources checked
    • cites [1] source

      Not checked in the free run.

    • cites [2] source

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    • cites [3] source

      Not checked in the free run.

  • Probably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.

    Premisecitation

    NER removes UV-induced lesions and is defective in xeroderma pigmentosum, which is characterized by UV hypersensitivity.

    “These lesions are removed through the nucleotide excision repair (NER) pathway which is defective in xeroderma pigmentosum (XP) syndrome characterized by UV hypersensitivity [2].”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [2] source

      Not checked in the free run.

  • May combine two claims.

    Interpretationown data

    Both TLS at stalled replication forks and gap-filling are active mechanisms for tolerance of UVC-induced DNA damage in human cells.

    “In conclusion, both TLS at stalled replication forks and gap-filling are active mechanisms for the tolerance of UVC-induced DNA damage in human cells”
    • Also stated in: § 1. Introduction · plain
      “Altogether, we report that according to the cellular genotype, both bypass at the replication fork and through a gap-filling pathway are active mechanisms”
    Quote in the paperSubstantial claim

  • Classified as probably not a substantial claim.

    Premisecitation

    H2AX is phosphorylated at serine 139 (γH2AX) in the vicinity of ssDNA, single-strand breaks, and double-strand breaks.

    “The variant histone H2AX is phosphorylated at serine 139 (forming ␥H2AX) in the vicinity of single-stranded DNA (ssDNA), DNA single-or double-strand breaks (SSBs and DSBs, respectively) [38][39][40].”
    Quote in the paperSubstantial claim0 of 3 sources checked
    • cites [38] source

      Not checked in the free run.

    • cites [39] source

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    • cites [40] source

      Not checked in the free run.

  • Probably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.

    Premisecitation

    TLS is the most studied tolerance pathway in human cells and involves specialized translesion polymerases that can use damaged DNA as templates.

    “The most studied tolerance pathway in human cells is translesion DNA synthesis (TLS), a process involving specialized translesion polymerases capable of using damaged DNA as replicative templates [7].”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [7] source

      Not checked in the free run.

  • May combine two claims.

    Premisecitation

    Polη ensures accurate replication of TT-CPDs, and its bypass may act at stalled replication forks and through post-replicative gap-filling.

    “It is well established that Pol␩ ensures accurate replication of TT-CPDs [21,22] and this bypass may act at the stalled replication fork [23,24] but also through a post-replicative gapfilling pathway [15,25].”
    Quote in the paperSubstantial claim0 of 3 sources checked
    • cites [21] source

      Not checked in the free run.

    • cites [23] source

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    • cites [15] source

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  • May combine two claims.

    Interpretationreasoning

    Because UV lesions are removed slowly, replication forks frequently encounter them and tolerance processes are activated.

    “Given the time required for full removal of UV-induced lesions, replication forks frequently encounter such distortions and processes that tolerate such replication barriers are activated.”
    Quote in the paperSubstantial claim

  • Probably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.

    Premisecitation

    Polη is the prototypic TLS polymerase and the only TLS polymerase known whose defects cause a human syndrome, the variant form of XP.

    “DNA polymerase ␩ (Pol␩, encoded by the POLH gene) is the prototypic TLS polymerase and the only TLS polymerase known which defects lead to a human syndrome [20], the variant form of XP (XP-V) [11].”
    Quote in the paperNot a substantial claim0 of 2 sources checked
    • cites [20] source

      Not checked in the free run.

    • cites [11] source

      Not checked in the free run.

  • May combine two claims.

    Interpretationcitation

    In UVC-irradiated XP-C cells, ATR activation might be triggered by accumulation of ssDNA gaps during replication, leading to mild and temporary G2-phase arrest.

    “In UVC-irradiated XP-C cells, ATR activation might be triggered by the accumulation of ssDNA gaps during DNA replication, leading to a mild and temporary G2-phase arrest, in agreement with previous work [18,19,24,50]”
    Quote in the paperSubstantial claim0 of 4 sources checked
    • cites [18] source

      Not checked in the free run.

    • cites [19] source

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    • cites [24] source

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    • cites [50] source

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  • May combine two claims.

    Interpretationown data

    ssDNA regions and γH2AX formation induced by UVC cannot be associated with prolonged replication fork arrest in XP-C cells.

    “ssDNA regions (Fig. 4D) and ␥H2AX formation (Fig. 3) induced by UVC cannot be associated with prolonged replication fork arrest in XP-C cells”
    Quote in the paperSubstantial claim

  • Probably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.

    Premisecitation

    GG-NER removes lesions throughout the genome in a manner dependent on XPC, whereas TC-NER targets lesions that stall RNA polymerase II.

    “Briefly, GG-NER removes lesions throughout the genome in a manner that depends on the XPC protein [3], whereas TC-NER targets lesions that stall RNA polymerase II.”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [3] source

      Not checked in the free run.

  • Classified as probably not a substantial claim.

    Premisecitation

    Only 60% of CPDs are excised within the first 24 hours after UVC exposure in normal human cells.

    “In contrast, only 60% of CPDs are excised within the first 24 h after UVC exposure in normal human cells [5,6].”
    Quote in the paperSubstantial claim0 of 2 sources checked
    • cites [5] source

      Not checked in the free run.

    • cites [6] source

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  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Premisecitation

    Polη may also be involved in bypass of 6-4PPs, as suggested by plasmid assays in yeast and human cells.

    “Pol␩ may also be involved in the bypass of 6-4PPs as suggested by plasmids assays performed both in yeast and human cells [26,27].”
    Quote in the paperNot a substantial claim0 of 2 sources checked
    • cites [26] source

      Not checked in the free run.

    • cites [27] source

      Not checked in the free run.

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Premisecitation

    NER is subdivided into global genome repair and transcription-coupled repair.

    “The NER pathway is subdivided into global genome repair (GG-NER) and transcription-coupled repair (TC-NER) [4].”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [4] source

      Not checked in the free run.

  • May combine two claims.

    Interpretationown data

    Human fibroblasts deficient in both XPC and Polη exhibit combined XP-C and XP-V phenotypes and are extremely sensitive to low-dose UVC.

    “Altogether, these results indicate that human fibroblasts deficient in both XPC and Pol␩ proteins exhibited the combined XP-C and XP-V phenotypes and were extremely sensitive to low-dose UVC irradiation.”
    Quote in the paperSubstantial claim

  • Classified as probably not a substantial claim. May combine two claims.

    Premisecitation

    Two models are proposed for TLS: at the blocked replication fork or via a post-replicative gap-filling mechanism.

    “Two models are currently proposed for TLS: at the blocked replication fork or via a post-replicative gap-filling mechanism [8,9].”
    Quote in the paperSubstantial claim0 of 2 sources checked
    • cites [8] source

      Not checked in the free run.

    • cites [9] source

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  • Classified as probably not a substantial claim.

    Premisecitation

    UVC sensitization by caffeine is a hallmark of the XP-V cell phenotype.

    “Because UVC sensitization by caffeine (CAF) is a hallmark of the XP-V cell phenotype [11,22,37]”
    Quote in the paperSubstantial claim0 of 3 sources checked
    • cites [11] source

      Not checked in the free run.

    • cites [22] source

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    • cites [37] source

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  • May combine two claims.

    Interpretationown data

    In the presence of Polη, gaps may form in the newly synthesized strand opposite UVC damage in the template strand, and these gaps are filled independently of replication fork progression.

    “In its presence, gaps may arise in the newly synthesized strand opposing the UVC damage in the template strand, which are filled independently of replication forks progression.”
    Quote in the paperSubstantial claim

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Premisecitation

    Some data suggest Polη can also play a role in bypass of 6-4PPs.

    “some data suggest that Pol␩ can also play a role in the bypass of 6-4PPs [26,27]”
    Quote in the paperNot a substantial claim0 of 2 sources checked
    • cites [26] source

      Not checked in the free run.

    • cites [27] source

      Not checked in the free run.

  • Probably not a substantial claim: may not pass S1 (asserted), S4 (based). May combine two claims.

    Interpretationreasoning

    6-4PP lesions are mainly bypassed through a post-replicative gap-filling process while CPDs are replicated by Polη directly at the replication fork.

    “One possibility is that 6-4PP lesions are mainly bypassed through a post-replicative gap-filling process while CPDs are replicated by Pol␩ directly at the replication fork.”
    Quote in the paperNot a substantial claim
    • Rests on an assumption: Polη rapidly replicates CPDs.
34 of 34

  • The paper relies on this without support.

    The XP-C cor cell line is an NER-proficient isogenic control for XP-C cells.

    “MRC5, a NERproficient clone derived from the XP4PA cell line, in which one copy of the causal XPC gene mutation has been corrected by homologous gene targeting, replaced by the XPC gene wild-type sequence (XP-C cor cells, unpublished results)”

  • The paper relies on this without support.

    BrdU immunostaining under non-denaturing conditions detects only single-stranded DNA molecules.

    “In these conditions, BrdU antibody identifies only singlestranded molecules, staining the cells when ssDNA are present.”

  • The paper relies on this without support.

    Polη efficiently bypasses only CPDs.

    “Pol␩ is known to bypass efficiently only this type of photoproduct.”

  • The paper relies on this without support.

    Polη rapidly replicates CPDs.

    “Pol␩ is known to rapidly replicate CPDs”

  • The paper relies on this without support.

    Most CPDs and 6-4PPs are not repaired in GG-NER-deficient cells.

    “most CPDs and 6-4PPs are not repaired in GG-NERdeficient cells”
5 of 5

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

Self-check

Percentages, sums and reported differences re-computed from the paper’s own numbers.

Each contradiction between two passages listed here was confirmed by an independent check.

  • DSB result points to an unrelated figure panel

    Minor

    The text cites Fig. 4C for double-strand breaks in cells without caffeine, but the caption identifies Fig. 4C as an immunostaining panel for γH2AX and RPA. The double-strand-break comet results are identified as Fig. 4B.

  • γH2AX result cites the SubG1 panel

    Minor

    The discussion cites Fig. 8C for increased γH2AX after ATR silencing, whereas the figure caption assigns SubG1 fractions to panel C and γH2AX measurements to panel D.

2 of 2

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Authors
Quinet, A., Vessoni, A. T., Rocha, C. R. R., Gottifredi, V., Biard, D., Sarasin, A., Menck, C. F. M., & Stary, A.
Affiliations
  • Université Paris-Sud (FR)
  • Universidade de São Paulo (BR)
  • Consejo Nacional de Investigaciones Científicas y Técnicas (AR)
  • Commissariat à l'Énergie Atomique et aux Énergies Alternatives (FR)
Corresponding author
  • Quinet, Annabel
  • Menck, Carlos F.M.
ORCID
Venue
DNA Repair
Publisher
Elsevier BV
Published
2014-02
Volume
14
Pages
27-38
ISSN
  • 1568-7856 (ISSN-L)
  • 1568-7864
DOI
10.1016/j.dnarep.2013.12.005
OpenAlex
W2106954306
Cited by
70
References
56
Citations by year
2026: 4 · 2025: 4 · 2023: 4 · 2022: 6 · 2021: 6 · 2020: 5 · 2019: 9 · 2018: 7 · 2017: 8 · 2016: 6 · 2015: 6 · 2014: 5
FWCI
3.42
Type
journal article
Language
en
Open access
Locations
  • DNA repair (publishedVersion)
  • PubMed (publishedVersion)
  • CONICET Digital (CONICET) (submittedVersion, cc-by-nc-sa)
Funders
  • Fundação de Amparo à Pesquisa do Estado de São Paulo
  • Coordenação de Aperfeiçoamento de Pessoal de Nível Superior
  • Conselho Nacional de Desenvolvimento Científico e Tecnológico
  • Ministère de l'Enseignement Supérieur et de la Recherche
  • Centre National de la Recherche Scientifique
  • Agencia Nacional de Promoción Científica y Tecnológica
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › DNA Repair Mechanisms
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Carcinogens and Genotoxicity Assessment
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › DNA and Nucleic Acid Chemistry
Keywords
DNA damage tolerance, UV-induced DNA damage, nucleotide excision repair, translesion synthesis, pol, gap filling, replication fork stalling, bypass, ATR-Chk1 pathway, S phase arrest, G2 cell cycle arrest, single-stranded DNA, UV-C irradiation, caffeine, cell death
MeSH terms
Y-Family DNA Polymerases, Caffeine, Cell Line, DNA Damage, DNA-Directed DNA Polymerase, DNA Repair, DNA Replication, DNA-Binding Proteins, DNA, Single-Stranded, Dose-Response Relationship, Radiation, Histones, Humans, Phosphorylation, Ultraviolet Rays, Genome, Human, G2 Phase, S Phase, DNA Breaks, Double-Stranded, DNA Breaks, Single-Stranded, Cell Cycle Checkpoints

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