XPA-Mediated Regulation of Global Nucleotide Excision Repair by ATR Is p53-Dependent and Occurs Primarily in S-Phase
Open accessAbstract
Cell cycle checkpoints play an important role in regulation of DNA repair pathways. However, how the regulation occurs throughout the cell cycle remains largely unknown. Here we demonstrate that nucleotide excision repair (NER) is regulated by the ATR/p53 checkpoint via modulation of XPA nuclear import and that this regulation occurs in a cell cycle-dependent manner. We show that depletion of p53 abrogated the UV-induced nuclear translocation of XPA, while silencing of Chk1 or MAPKAP Kinase-2 (MK2) had no effect. Inhibition of p53 transcriptional activities and silencing of p53-Ser15 phosphorylation also reduced the damage-induced XPA nuclear import. Furthermore, in G1-phase cells the majority of XPA remained in the cytoplasm even after UV treatment. By contrast, while most of the XPA in S-phase cells was initially located in the cytoplasm before DNA damage, UV irradiation stimulated bulk import of XPA into the nucleus. Interestingly, the majority of XPA molecules always were located in the nucleus in G2-phase cells no matter whether the DNA was damaged or not. Consistently, the UV-induced Ser15 phosphorylation of p53 occurred mainly in S-phase cells, and removal of cyclobutane pyrimidine dimers (CPDs) was much more efficient in S-phase cells than in G1-phase cells. Our results suggest that upon DNA damage in S phase, NER could be regulated by the ATR/p53-dependent checkpoint via modulation of the XPA nuclear import process. In contrast, the nuclear import of XPA in G(1) or G(2) phase appears to be largely independent of DNA damage and p53.
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Nuclear import of XPA after UV irradiation or cisplatin treatment is ATR-dependent in normal fibroblasts and p53-proficient cancer cells, and also depends on p53 transcriptional activity.
“Li et al. demonstrated that the nuclear import of XPA in response to UV irradiation or cisplatin treatment is ATR-dependent in normal fibroblasts and in cancer cells that are p53 proficient; XPA import also is dependent on the transcriptional activity of p53 in these cells 69, 70.”
From Xeroderma Pigmentosa Group A (XPA), Nucleotide Excision Repair and Regulation by ATR in Response to Ultraviolet Irradiation (2017) · cites this paper as [69]
XPA occurs predominantly in the cytoplasm of normal mammalian cells and is translocated to the nucleus after DNA damage, especially UV irradiation.
“However, biochemical fractionation of millions of cells into nuclear vs. cytoplasmic fractions revealed that XPA occurs predominantly in the cytoplasm of normal mammalian cells and that it is translocated to the nucleus in response to DNA damage, especially from UV irradiation 67–70.”
From Xeroderma Pigmentosa Group A (XPA), Nucleotide Excision Repair and Regulation by ATR in Response to Ultraviolet Irradiation (2017) · cites this paper as [69]
Efficient NER removal of damage depends on ATR kinase activity in p53-proficient cells, but the repair process appears ATR-independent in p53-deficient cells.
“Although efficient NER removal of the damage was dependent on ATR kinase activity in p53-proficient (p53+/+) cells the repair process seemed to be ATR-independent in p53-deficient (p53−/−) cells 69, 70, 77.”
From Xeroderma Pigmentosa Group A (XPA), Nucleotide Excision Repair and Regulation by ATR in Response to Ultraviolet Irradiation (2017) · cites this paper as [69]
The p53 status of cells significantly influences the role of ATR in regulating DNA repair after UV or cisplatin damage.
“Interestingly, the p53 status of cells significantly influences the role of ATR in regulating DNA repair after UV or cisplatin damage.”
From Xeroderma Pigmentosa Group A (XPA), Nucleotide Excision Repair and Regulation by ATR in Response to Ultraviolet Irradiation (2017) · cites this paper as [69]
ATM, Chk1, and MK2 appear not to have a role in XPA nuclear import in either p53+/+ or p53−/− cells.
“The cell cycle checkpoint kinases ATM, Chk1 and MK2 appear not to have a role in XPA nuclear import in p53+/+ nor p53−/− cells 69, 70.”
From Xeroderma Pigmentosa Group A (XPA), Nucleotide Excision Repair and Regulation by ATR in Response to Ultraviolet Irradiation (2017) · cites this paper as [69]
Importin-α7 functions independently of DNA damage and ATR kinase activation, perhaps reflecting G2-phase XPA import.
“In contrast, importin-α7 functioned independent of DNA damage and ATR kinase activation, perhaps reflecting the observed nuclear import of XPA in the G2 phase irrespective of UV exposure 69.”
From Xeroderma Pigmentosa Group A (XPA), Nucleotide Excision Repair and Regulation by ATR in Response to Ultraviolet Irradiation (2017) · cites this paper as [69]
There may be two stages of XPA nuclear import: one occurs naturally in the absence of DNA damage, and another massive transport (particularly in S-phase) is initiated by specific DNA damage signaling.
“These observations indicate that there maybe two stages of XPA nuclear import: one occurs naturally in the absence of DNA damage, and another, the massive transport (particularly in S-phase), is initiated by specific DNA damage signaling [24], [32], [33].”
From UV-Induced Nuclear Import of XPA Is Mediated by Importin-α4 in An ATR-Dependent Manner (2013) · cites this paper as [33]
The DNA damage-induced nuclear import of cytoplasmic XPA for NER during S-phase is a DNA damage checkpoint-dependent process mediated by ATR and p53.
“It was shown previously that the DNA damage-induced nuclear import of cytoplasmic XPA for NER during S-phase is a DNA damage checkpoint-dependent process mediated by ataxia telangiectasia and Rad3-related (ATR) protein and p53 tumor suppressor protein [24], [25], [33].”
From UV-Induced Nuclear Import of XPA Is Mediated by Importin-α4 in An ATR-Dependent Manner (2013) · cites this paper as [33]
XPA localization to the nucleus depends on DNA damage and cell cycle stage.
“XPA has an N-terminal NLS (Figure 1), but its localization to the nucleus where it functions also depends on DNA damage and cell cycle stage [24], [32], [33].”
From UV-Induced Nuclear Import of XPA Is Mediated by Importin-α4 in An ATR-Dependent Manner (2013) · cites this paper as [33]
The dependence of XPA-importin-α4 binding on ATR may occur via ATR regulation of other cytoplasmic factors involved in regulating the XPA-importin-α4 binding.
“This suggests that the dependence of the XPA-importin-α4 binding on ATR may occur via ATR regulation of other cytoplasmic factors involved in regulating the XPA-importin-α4 binding [24], [33].”
From UV-Induced Nuclear Import of XPA Is Mediated by Importin-α4 in An ATR-Dependent Manner (2013) · cites this paper as [33]
In G2-phase cells, XPA is localized to the nucleus regardless of DNA damage.
“In G2-phase cells, XPA was localized to the nucleus regardless of DNA damage [33].”
From UV-Induced Nuclear Import of XPA Is Mediated by Importin-α4 in An ATR-Dependent Manner (2013) · cites this paper as [33]
The DNA damage-induced nuclear import of XPA is cell cycle dependent, primarily occurring in S phase.
“the DNA damage-induced nuclear import of XPA was cell cycle dependent, primarily occurring in S phase [33].”
From UV-Induced Nuclear Import of XPA Is Mediated by Importin-α4 in An ATR-Dependent Manner (2013) · cites this paper as [33]
XPA is predominantly localized to the nucleus in unstressed G2-phase cells.
“we previously reported that XPA was predominantly localized to the nucleus in unstressed G2-phase cells [33].”
From UV-Induced Nuclear Import of XPA Is Mediated by Importin-α4 in An ATR-Dependent Manner (2013) · cites this paper as [33]
The observations of nucleus-only XPA in immunofluorescence reports may not be inconsistent with the results of this study because XPA subcellular localization in unstressed cells is cell cycle-dependent.
“the observations may not be inconsistent with the results of this study since XPA subcellular localization in unstressed cells is cell cycle-dependent [33].”
From UV-Induced Nuclear Import of XPA Is Mediated by Importin-α4 in An ATR-Dependent Manner (2013) · cites this paper as [33]
Immunofluorescence images may accurately depict XPA distribution within an individual cell but do not reflect the subcellular localization of XPA within a population of cells, whereas biochemical fractionation studies represent the average XPA distribution within millions of cells.
“Though immunofluorescence images may accurately depict XPA distribution within an individual cell they do not reflect the subcellular localization of XPA within a population of cells as do our biochemical fractionation studies which represent the average XPA distribution within millions of cells [24], [32], [33].”
From UV-Induced Nuclear Import of XPA Is Mediated by Importin-α4 in An ATR-Dependent Manner (2013) · cites this paper as [33]
The basal level of nuclear XPA in the fractionation assays may vary somewhat between experiments, likely due to culture variations affecting the proportion of cells in the G2 phase.
“Even the basal level of nuclear XPA in the fractionation assays may vary somewhat between experiments, likely due to culture variations affecting the proportion of cells in the G2 phase [32], [33].”
From UV-Induced Nuclear Import of XPA Is Mediated by Importin-α4 in An ATR-Dependent Manner (2013) · cites this paper as [33]
Since the DNA damage-induced nuclear import of XPA occurs primarily in S-phase, the inhibition is expected to be specific to replicative cells, typically cancer cells, without interruption of XPA functions in cells in other cell cycle phases.
“Since the DNA damage-induced nuclear import of XPA occurs primarily in S-phase [33], the inhibition is expected to be specific to replicative cells, typically cancer cells, without interruption of XPA functions in cells in other cell cycle phases.”
From UV-Induced Nuclear Import of XPA Is Mediated by Importin-α4 in An ATR-Dependent Manner (2013) · cites this paper as [33]
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Cartwright, B. M., Musich, P. R., & Zou, Y. (2017) · Current human cell research and applications · doi:10.1007/978-981-10-7296-3_6 · Cited by 3 · see citing works
Self-citationCharacterization of the multifunctional XPG protein during Nucleotide-excision-repair
Schubert, S. (2014) · doi:10.53846/goediss-4515 · Cited by 2 · see citing works
Novel Roles of Replication Protein A Phosphorylation in the Cellular Response to DNA Damage
Serrano, M. A. (2013) · Digital Commons - East Tennessee State University (East Tennessee State University)
Self-citationTaira, M., Kagiya, T., Sasaki, M., & Kimura, S. (2011) · Nano biomedicine · doi:10.11344/nano.3.294
Lima, L. C. D. A. (2014) · Digital Library of Theses and Dissertations (Universidade de São Paulo) · doi:10.11606/t.42.2014.tde-28112014-100235
Beardmore, R. (2015) · Bangor University Research Portal (Bangor University)
Musich, P. R., Li, Z., Shell, S. M., & Zou, Y. (2018) · DNA repair · doi:10.1016/j.dnarep.2018.01.001
Self-citation
- Authors
- Li, Z., Musich, P. R., Serrano, M. A., Dong, Z., & Zou, Y.
- Affiliations
- East Tennessee State University (US)
- Corresponding author
- Zou, Yue
- Venue
- PLoS ONE
- Publisher
- Public Library of Science (PLoS)
- Published
- 2011-12-12
- Volume
- 6
- Issue
- 12
- Pages
- e28326
- ISSN
- 1932-6203 (ISSN-L)
- PMC
- PMC3236200
- OpenAlex
- W1979028355
- Cited by
- 38
- References
- 47
- Citations by year
- 2022: 1 · 2021: 2 · 2020: 1 · 2018: 4 · 2017: 5 · 2016: 3 · 2015: 6 · 2014: 5 · 2013: 5 · 2012: 5
- FWCI
- 2.08
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- PLoS ONE (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Digital Commons - East Tennessee State University (East Tennessee State University) (submittedVersion, cc-by)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- National Institutes of Health
- National Cancer Institute (R56CA086927, R01CA086927, CA-86927)
- National Institute of General Medical Sciences (R15GM083307, GM083307)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › DNA Repair Mechanisms
- Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Nuclear Structure and Function
- Keywords
- XPA, nucleotide excision repair, ATR, p53, cell cycle checkpoints, p53 Ser15 phosphorylation, UV-induced DNA damage, cyclobutane pyrimidine dimers, S phase, G1 phase, G2 phase, Chk1, MAPKAPK2
- MeSH terms
- Checkpoint Kinase 1, MAP-Kinase-Activated Kinase 2, Cell Nucleus, DNA Damage, DNA Repair, Humans, Phosphorylation, Phosphoserine, Protein Kinases, Pyrimidine Dimers, Subcellular Fractions, Ultraviolet Rays, Tumor Suppressor Protein p53, G1 Phase, S Phase, Protein Serine-Threonine Kinases, Cell Cycle Proteins, Protein Transport, Active Transport, Cell Nucleus, Cell Line, Tumor, Intracellular Signaling Peptides and Proteins, Xeroderma Pigmentosum Group A Protein, Cell Cycle Checkpoints, Ataxia Telangiectasia Mutated Proteins
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