Distribution and repair of O6-methylguanine in different fractions of rat liver DNA after dimethylnitrosamine administration

Galbraith, A.I.; Itzhaki, Ruth F.; Craig, A. W.; Margison, Geoffrey P.

doi:10.1016/0009-2797(80)90153-2

Cited by 6 publications

(2 citation statements)

References 19 publications

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“…When rodent cells treated with the alkylating agent dimethylsulfate (DMS) are analyzed for preferential DNA repair, no significant difference was observed between transcribed and nontranscribed genetic regions (Scicchitano and Hanawalt, 1990). This is in agreement with other studies showing that there was little difference in the repair of alkali-sensitive sites in collagen I and ␤-globin genes of N-methyl-N-nitro-N-nitrosoguanidine (MNNG)-treated confluent human cells, and that Nmethylpurines are removed uniformly from rat liver chromatin (Galbraith et al, 1980;Ryan et al, 1986). Overall, the weight of evidence supports the idea that bulky DNA damage, which can block transcription and replication, is repaired preferentially by TCR, whereas small base modifications, such as those produced by monofunctional DNA alkylating agents, are removed from active and inactive genes at similar rates.…”

Section: Nucleotide Excision Repair and Base Excision Repairsupporting

confidence: 88%

Relative Base Excision Repair in Xiphophorus Fish Tissue Extracts

Walter

Sung

Obermoeller

et al. 2001

Marine Biotechnology

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To begin characterizing DNA repair capability among Xiphophorus species, we adapted oligonucleotide-based DNA repair assays to extracts of fish tissues. Here, we report the initial results of relative base excision repair (BER) capability among 3 inbred Xiphophorus fish lines representing 2 species (X. maculatus and X. couchianus), and interspecies hybrid F(1) animals produced by crossing them. Overall, data from uracil- N-glycosylase (UNG)-initiated BER assay (UNG-BER) indicate that brain tissue extracts generally possess higher BER activity than do gill and liver extracts. UNG-BER activities in gill and liver extracts were similar. The BER activity in the tissues of F(1) interspecies hybrids followed the activity pattern of the X. couchianus parent in gill and liver extracts, was similar to the X. maculatus parent in brain extracts, but exhibited a reduced repair capacity in gill tissue extracts compared with either parent. We discuss the use of oligonucleotide-based DNA repair assays to elucidate the role that inheritance of DNA repair potential may play in susceptibility to disease and tumorigenesis in the intact organism.

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Section: Nucleotide Excision Repair and Base Excision Repairsupporting

confidence: 88%

Relative Base Excision Repair in Xiphophorus Fish Tissue Extracts

Walter

Sung

Obermoeller

et al. 2001

Marine Biotechnology

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“…While Galbraith et al (16) observed no differences in the methylation or repair at the 06 position of guanine in various fractions, Ryan et al (17) reported a significantly higher rate of removal of 06-methylguanine in active regions of chromatin. They also reported that removal of Nmethylpurines, unlike 06-methylguanine, was the same in the different fractions of chromatin they studied.…”

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confidence: 99%

Repair of N-methylpurines in specific DNA sequences in Chinese hamster ovary cells: absence of strand specificity in the dihydrofolate reductase gene.

Scicchitano

Hanawalt

1989

Proc. Natl. Acad. Sci. U.S.A.

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We have developed a quantitative method for examining the removal ofN-methylpurines from specific genes to investigate their possible differential repair throughout the genome. Chinese hamster ovary cells were exposed to dimethyl sulfate, and the isolated DNA was treated with an appropriate restriction endonuclease. The DNA was heated to convert remaining N-methylpurines to apurinic sites to render them alkaline-labile. Duplicate samples heated in the presence of methoxyamine to protect the apurinic sites from alkaline hydrolysis provided controls to assess total DNA. After alkaline hydrolysis, agarose gel electrophoresis, Southern transfer, and probing for the fragment of interest, the ratios of band intensities of the test DNA sample to its methoxyamine-treated control counterpart were calculated to yield the percentage of fragments containing no alkaline-labile sites. The frequency of N-methylpurines was measured at different times after dimethyl sulfate treatment to study repair. We found no differences between the rates of repair of N-methylpurines in the active dihydrofolate reductase gene and a nontranscribed region located downstream from it in treated cells. Also, similar rates of repair were observed in the transcribed and nontranscribed strands of the gene, in contrast to previous results for the removal of cyclobutane pyrimidine dimers. Thus, there does not appear to be a coupling of N-methylpurine repair to transcription in Chinese hamster ovary cells. However, the repair in the dihydrofolate reductase domain appears to be somewhat more efficient than that in the genome overall. Our method permits the quantifying at the defined gene level of abasic sites or of any DNA adduct that can be converted to them.The excision-repair of structure-distorting DNA lesions in mammalian chromatin is generally heterogeneous (reviewed in refs. 1-3). Cyclobutane pyrimidine dimers are excised rapidly from the active dihydrofolate reductase (DHFR) gene but persist in the bulk DNA in UV-irradiated Chinese hamster ovary (CHO) cells (4). Furthermore, efficient DNA repair is selective for the transcribed strand of the DHFR gene (5). Some bulky chemical DNA adducts also exhibit differential repair in mammalian cells, including aflatoxin B1 and psoralen photoadducts, which are removed less efficiently from the unexpressed a-satellite DNA sequences than from the bulk DNA in African green monkey cells (6-8).Within the DHFR gene in human cells, the interstrand cross-linking of DNA by psoralen diadducts is repaired at a faster rate than are psoralen monoadducts in the same region (9). Thus, efficiency of DNA repair may be affected by a variety of factors, including the nature of the damage, its location within the genome, the state of expression of the affected DNA sequences, and the chromatin configuration of the region under study.Simple methylating agents, such as dimethyl sulfate (DMS), produce a variety ofdamaged bases in DNA of which 7-methylguanine and 3-methyladenine constitute approximately 90%o of the alteratio...

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Lack of sequence-specific removal of N-methylpurines from cellular DNA

Scicchitano

Hanawalt

1990

Mutation Research/Fundamental and Molecular Mechanisms of Mutag

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Distribution and repair of O6-methylguanine in different fractions of rat liver DNA after dimethylnitrosamine administration

Cited by 6 publications

References 19 publications

Relative Base Excision Repair in Xiphophorus Fish Tissue Extracts

Relative Base Excision Repair in Xiphophorus Fish Tissue Extracts

Repair of N-methylpurines in specific DNA sequences in Chinese hamster ovary cells: absence of strand specificity in the dihydrofolate reductase gene.

Lack of sequence-specific removal of N-methylpurines from cellular DNA

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