Quantitation and Visualization of Ultraviolet‐Induced DNA Damage Using Specific Antibodies: Application to Pigment Cell Biology

Kobayashi, Nobuhiko; Katsumi, Sachiko; Imoto, Kyoko; Nakagawa, Akemi; Miyagawa, Sachiko; Furumura, Minao; Mori, Toshio

doi:10.1034/j.1600-0749.2001.140204.x

Cited by 63 publications

(56 citation statements)

References 50 publications

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“…The involvement of p53 in removing the UV photoproducts in Global Genomic Repair, a sub pathway of Nucleotide Excision Repair has been documented with different assays such as Unscheduled DNA synthesis (UDS), ELISA, Slot blot etc. 27,28 Using photoproduct specific antibodies in immunofluorescence assays, we investigated the removal of CPDs or 6-4 PP in the absence of functional p53 by infecting the U2OS cells with Ad-E6 vectors prior to UV exposure (Fig. 2).…”

Section: Resultsmentioning

confidence: 99%

Cooperation between BRCA1 and p53 in repair of cyclobutane pyrimidine dimers

Seyhan¹,

Mori²,

El‐Deiry³

2005

Cancer Biology & Therapy

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DNA repair defects can predispose to cancer development and progression. We previously showed that the breast and ovarian cancer susceptibility gene product BRCA1, through p53, upregulates expression of the XPE gene DDB2, encoding the nucleotide excision repair protein p48. Both XPE and XPC are p53 target genes containing p53 response elements. To further explore the role of BRCA1 and p53 in repair of photoproducts, we eliminated wild type p53 from U2OS osteosarcoma cells and found that cyclobutane pyrimidine dimer (CPD) repair was markedly impaired following UV damage whereas repair of 6-4 photoproduct (6-4 PP) occurred efficiently. Overexpression of p53 in p53-null Calu-6 cells also enhanced CPD repair. In HCC1937 breast cancer cells, harboring mutant BRCA1 and p53 genes, repair of CPD was markedly impaired. Reintroduction of either p53 or BRCA1 using adenovirus vectors into HCC1937 alone had little effect on repair of CPD whereas the combination of p53 and BRCA1 resulted in efficient repair of CPD. Thus there appears to be a cooperative effect between p53 and BRCA1 that may involve induction of repair proteins, inhibition of p53-induced cell death by BRCA1 with altered p53 selectivity towards repair pathways and/or p53-independent effects of BRCA1 on CPD repair.

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Section: Resultsmentioning

confidence: 99%

Cooperation between BRCA1 and p53 in repair of cyclobutane pyrimidine dimers

Seyhan¹,

Mori²,

El‐Deiry³

2005

Cancer Biology & Therapy

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“…This procedure was described previously. [46][47] Briefly, 2 x 10 4 cells seeded/well in 24 well culture plates were infected with Ad-LacZ or Ad-AS-BRCA1 at 40 MOI for 24 hrs, then irradiated with 20 J/m 2 UVC. Cells were fixed immediately, at 6 hrs, 24 hrs, and 48 hrs after irradiation with cold (4°C) methanol-acetic acid (3:1) for one hour.…”

Section: Methodsmentioning

confidence: 99%

BRCA1 Transcriptionally Regulates Damaged DNA Binding Protein (DDB2) In the DNA Repair Response Following UV-Irradiation

Takimoto¹,

MacLachlan²,

Dicker³

et al. 2002

Cancer Biology & Therapy

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© 2 0 0 2 L a n d e s B i o s c i e n c e . N o t f o r d i s t r i b u t i o n .[Cancer Biology & ABSTRACTThe p53 and BRCA1 tumor suppressors are involved in repair processes and may cooperate to transactivate certain genes, including p21WAF1/CIP1 and GADD45. We find that the Xeroderma Pigmentosum Complementation group E (XPE) mutated Damaged-DNA binding protein p48 (DDB2) is upregulated by BRCA1 in a p53-dependent manner following UVC, Adriamycin, or Cisplatin exposure. BRCA1 enhances p53 binding to the DDB2 promoter in vivo as well as p53-dependent transactivation of DDB2 promoterreporter constructs through a classical p53 DNA responsive element. Antisense abrogation of BRCA1 expression abrogates upregulation of DDB2 after UVC or cisplatin exposure. Using a host cell reactivation assay, DNA repair activity is more significantly restored by introduction of BRCA1 into wt as compared to DDB2-deficient cells. Furthermore disappearance of the photoproducts cyclobutane pyrimidine dimer (CPD) and 6-4 photoproduct (6-4PP) was delayed by antisense abrogation of BRCA1 expression in UV-exposed human cells. Thus the DNA repair function of BRCA1 may be attributed in part to p53-dependent transcriptional induction of DDB2. Loss of BRCA1-dependent DDB2 repair function may contribute to cancer susceptibility and cellular sensitivity to DNA damage.

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“…DNA was extracted from 100 mg pooled leaf tissue using a genomic DNA isolation kit (Aquapure, Bio-Rad Laboratories), the yield was determined by spectrophotometric A 260 , and the DNA resuspended in phosphate-buffered saline at 0.2 mg mL 21 . CPDs were detected by an ELISA procedure using 96-well microtitre plates with four well replicates per sample, monoclonal anti-CPD antibodies (Mori et al, 1991;Kobayashi et al, 2001; TMD-2, MBL International), peroxidasestreptavidin, and spectrophotometric A 492 according to the manufacturer's instructions.…”

Section: Elisa Assaymentioning

confidence: 99%

UV-Induced DNA Damage Promotes Resistance to the Biotrophic Pathogen Hyaloperonospora parasitica in Arabidopsis

et al. 2008

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Plant innate immunity to pathogenic microorganisms is activated in response to recognition of extracellular or intracellular pathogen molecules by transmembrane receptors or resistance proteins, respectively. The defense signaling pathways share components with those involved in plant responses to UV radiation, which can induce expression of plant genes important for pathogen resistance. Such intriguing links suggest that UV treatment might activate resistance to pathogens in normally susceptible host plants. Here, we demonstrate that pre-inoculative UV (254 nm) irradiation of Arabidopsis (Arabidopsis thaliana) susceptible to infection by the biotrophic oomycete Hyaloperonospora parasitica, the causative agent of downy mildew, induces dose-and timedependent resistance to the pathogen detectable up to 7 d after UVexposure. Limiting repair of UV photoproducts by postirradiation incubation in the dark, or mutational inactivation of cyclobutane pyrimidine dimer photolyase, (6-4) photoproduct photolyase, or nucleotide excision repair increased the magnitude of UV-induced pathogen resistance. In the absence of treatment with 254-nm UV, plant nucleotide excision repair mutants also defective for cyclobutane pyrimidine dimer or (6-4) photoproduct photolyase displayed resistance to H. parasitica, partially attributable to short wavelength UV-B (280-320 nm) radiation emitted by incubator lights. These results indicate UV irradiation can initiate the development of resistance to H. parasitica in plants normally susceptible to the pathogen and point to a key role for UV-induced DNA damage. They also suggest UV treatment can circumvent the requirement for recognition of H. parasitica molecules by Arabidopsis proteins to activate an immune response.

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Quantitation and Visualization of Ultraviolet‐Induced DNA Damage Using Specific Antibodies: Application to Pigment Cell Biology

Cited by 63 publications

References 50 publications

Cooperation between BRCA1 and p53 in repair of cyclobutane pyrimidine dimers

Cooperation between BRCA1 and p53 in repair of cyclobutane pyrimidine dimers

BRCA1 Transcriptionally Regulates Damaged DNA Binding Protein (DDB2) In the DNA Repair Response Following UV-Irradiation

UV-Induced DNA Damage Promotes Resistance to the Biotrophic Pathogen Hyaloperonospora parasitica in Arabidopsis

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