+ Site Statistics
References:
52,654,530
Abstracts:
29,560,856
PMIDs:
28,072,755
+ Search Articles
+ Subscribe to Site Feeds
Most Shared
PDF Full Text
+ PDF Full Text
Request PDF Full Text
+ Follow Us
Follow on Facebook
Follow on Twitter
Follow on LinkedIn
+ Translate
+ Recently Requested

Repair of DNA damage in mammalian cells after treatment with UV and dimethyl sulphate: Discrimination between nucleotide and base excision repair by their temperature dependence



Repair of DNA damage in mammalian cells after treatment with UV and dimethyl sulphate: Discrimination between nucleotide and base excision repair by their temperature dependence



Mutation Research 407(2): 87-96



Alkylating agents have been reported to give rise to both short and long patches of repair. The reason for the different patch sizes is not known. One possibility is that alkylating agents can trigger both base and nucleotide excision repair. Another possibility is that base excision repair itself can result in different patch sizes. Recognition and incision at lesions is the rate limiting step in excision repair. In order to discriminate between base and nucleotide excision repair it would be desirable to be able to distinguish between different incision activities. In order to accurately measure incision rates, the rejoining of the strand-breaks formed must be inhibited. We have used two inhibitors, aphidicolin and 3-aminobenzamide. Aphidicolin, an inhibitor of DNA polymerases alpha/delta/epsilon. caused accumulation of single-strand breaks both after UV and dimethylsulphate. 3-Aminobenzamide, an inhibitor of poly(ADP-ribose)-polymerase caused accumulation of single-strand breaks only after alkylating agents and is thus specific for base excision repair. Enzymatic activities can be characterised by their activation energy. In order to discriminate between base and nucleotide excision repair the temperature dependence of incision activities was determined. When the temperature is decreased, the incision rate is reduced to a larger extent for UV than for DMS-induced repair. Incisions in UV-irradiated cells are practically cut off at temperatures of 15 degrees C and below, whereas DMS-exposed cells still are actively repairing at this temperature. In DMS treated cells the temperature dependence was the same whether aphidicolin or 3-aminobenzamide was used, speaking against an involvement of nucleotide excision repair. In addition, cell lines deficient in nucleotide excision repair responded in the same way to aphidicolin after DMS treatment as normal cells and were able to make incisions at 15 degrees C. This indicates that nucleotide excision repair is not to any significant amount involved in repair of DNA damage induced by a methylating agent.

(PDF emailed within 0-6 h: $19.90)

Accession: 009338225

Download citation: RISBibTeXText

PMID: 9637237

DOI: 10.1016/s0921-8777(97)00062-1


Related references

Discrimination between base and nucleotide excision repair by the difference in temperature dependence of incision activities. Mutagenesis 7(5): 388-389, 1992

DNA repair in higher plants; photoreactivation is the major DNA repair pathway in non-proliferating cells while excision repair (nucleotide excision repair and base excision repair) is active in proliferating cells. Nucleic Acids Research 32(9): 2760-2767, 2004

Involvement of the nucleotide excision repair proteins in the removal of oxidative DNA base damage in mammalian cells. Neoplasma 50(6): 389-395, 2003

Overlapping specificities of base excision repair, nucleotide excision repair, recombination, and translesion synthesis pathways for DNA base damage in Saccharomyces cerevisiae. Molecular and Cellular Biology 19(4): 2929-2935, 1999

Effects of nitrous acid treatment on the survival and mutagenesis of Escherichia coli cells lacking base excision repair (hypoxanthine-DNA glycosylase-ALK A protein) and/or nucleotide excision repair. Mutagenesis 12(1): 23-28, 1997

Mammalian DNA base excision repair proteins: their interactions and role in repair of oxidative DNA damage. Toxicology 193(1-2): 43-65, 2003

Discontinuous DNA replication in a lig-7 strain of Escherichia coli is not the result of mismatch repair, nucleotide-excision repair, or the base-excision repair of DNA uracil. Biochemical and Biophysical Research Communications 165(2): 685-688, 1989

Differential regulation of base and nucleotide excision repair in mammalian cells. Basic Life Sciences 38: 159-170, 1986

DNA damage recognition during nucleotide excision repair in mammalian cells. Biochimie (Paris) 81(1-2): 39-44, 1999

DNA damage recognition and nucleotide excision repair in mammalian cells. Cold Spring Harbor Symposia on Quantitative Biology 65: 173-182, 2003

Base excision repair of mitochondrial DNA damage in mammalian cells. Progress in Nucleic Acid Research and Molecular Biology 68: 273-284, 2001

Impact of Single Nucleotide Polymorphisms of Base Excision Repair Genes on DNA Damage and Efficiency of DNA Repair in Recurrent Depression Disorder. Molecular Neurobiology 54(6): 4150-4159, 2016

An Integrated Approach for Analysis of the DNA Damage Response in Mammalian Cells: NUCLEOTIDE EXCISION REPAIR, DNA DAMAGE CHECKPOINT, AND APOPTOSIS. Journal of Biological Chemistry 290(48): 28812-28821, 2016