Mutation Research/DNA Repair Reports最新文献_第4页

Contents of volume 193 (1988) 第193卷(1988年)目录

Mutation Research/DNA Repair Reports Pub Date : 1988-05-01 DOI: 10.1016/0167-8817(88)90038-7

引用次数: 0

Role of active oxygen species in metal-induced DNA strand breakage in human diploid fibroblasts 活性氧在金属诱导的人二倍体成纤维细胞DNA链断裂中的作用

Mutation Research/DNA Repair Reports Pub Date : 1988-05-01 DOI: 10.1016/0167-8817(88)90034-X

Ronald D. Snyder

引用次数: 97

Mutants of Aspergillus nidulans with increased resistance to the alkylating agent, N-methyl-N′-nitro-N-nitrosoguanidine 对烷基化剂n -甲基-n′-硝基-n -亚硝基胍抗性增强的中性曲霉突变体

Mutation Research/DNA Repair Reports Pub Date : 1988-05-01 DOI: 10.1016/0167-8817(88)90035-1

P. Hooley, S.G. Shawcross, P. Strike

引用次数: 4

Repair of alkylation damage in the fungus Aspergillus nidulans 木质素曲霉烷基化损伤的修复

Mutation Research/DNA Repair Reports Pub Date : 1988-05-01 DOI: 10.1016/0167-8817(88)90036-3

Richard A. Swirski, Susan G. Shawcross, Barry M. Faulkner, Peter Strike

{"title":"Repair of alkylation damage in the fungus Aspergillus nidulans","authors":"Richard A. Swirski, Susan G. Shawcross, Barry M. Faulkner, Peter Strike","doi":"10.1016/0167-8817(88)90036-3","DOIUrl":"10.1016/0167-8817(88)90036-3","url":null,"abstract":"<div>The repair of alkylation damage in Aspergillus nidulans was investigated. We have assayed soluble protein fractions for enzymes known to be involved in the repair of this type of damage in DNA. The presence of a glycosylase activity that can remove 3-methyladenine from DNA was demonstrated, as well as a DNA methyltransferase activity that appears to act against O6-methylguanine.In addition to this approach, a series of mutants were isolated which display increased sensitivity to alkylating agents (sag mutants). 5 such mutants were further characterized, and at least 4 are shown to map to genes which have not previously been characterized. The behaviour of double mutant combinations demonstrates the existence of at least 2 pathways for the repair of alkylation damage. The majority of the sag mutants (sagA1, sagB2, sag4 and sagE5) exhibit an increased sensitivity to a range of alkylating agents, but not to UV light, while sagC3, when irradiated at the germling stage, also shows sensitivity to UV. None of the mutants isolated are defective in either the 3-methyladenine DNA glycosylase activity, or the DNA methyltransferase activity, and the nature of the defects in these strains remains to be determined.</div>","PeriodicalId":100936,"journal":{"name":"Mutation Research/DNA Repair Reports","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"1988-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/0167-8817(88)90036-3","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"13598262","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 9

Frameshift lesions induced by oxazolopyridocarbazoles are recognized by the mismatch repair system in Escherichia coli 由恶唑吡啶咔唑引起的移码损伤被大肠杆菌错配修复系统识别

Mutation Research/DNA Repair Reports Pub Date : 1988-05-01 DOI: 10.1016/0167-8817(88)90037-5

Brigitte René, Christian Auclair, Claude Paoletti

引用次数: 5

pH induced damage and repair in E. coli pH诱导大肠杆菌的损伤和修复

Mutation Research/DNA Repair Reports Pub Date : 1988-05-01 DOI: 10.1016/0167-8817(88)90032-6

Javed Musarrat, Masood Ahmad

{"title":"pH induced damage and repair in E. coli","authors":"Javed Musarrat, Masood Ahmad","doi":"10.1016/0167-8817(88)90032-6","DOIUrl":"10.1016/0167-8817(88)90032-6","url":null,"abstract":"<div>Escherichia coli lost its colony-forming ability when suspended in Tris/NaOH or Tris/Mg2+ buffers of pH 10.0 and 4.0, respectively. A significant decrease in the survival of radiation-sensitive mutants recA, polA, res, rer and lexA was observed as compared to their wild-type counterpart under these conditions. The alkali-injured cells were found to recover when incubated at 37°C for 2 h in 0.05 M phosphate buffer of pH 8.0, whereas no such liquid holding recovery was observed in recA and lexA mutants. Recovery in phosphate buffer was not affected by metabolic inhibitors. As a result of alkali treatment, the sensitivity of bacteria to ultraviolet light (UV) was enhanced. However, on incubation for 2 h in recovery buffer at 37°C, the bacteria regained partial UV resistance. Bacteria exposed to alkaline environment exhibited an enhanced level of mutagenesis. Contrary to the treated wild-type, the mutants recA and lexA did not exhibit any increase in the mutation frequency. Alkali treatment to GC → AT transition mutants of Salmonella typhimurium, TA102 and TA104 resulted in the highest number of revertants per plate.</div>","PeriodicalId":100936,"journal":{"name":"Mutation Research/DNA Repair Reports","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"1988-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/0167-8817(88)90032-6","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"14412745","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 5

Survival and mutagenic effects of 5-azacytidine in Escherichia coli 5-氮杂胞苷在大肠杆菌中的存活及致突变作用

Mutation Research/DNA Repair Reports Pub Date : 1988-05-01 DOI: 10.1016/0167-8817(88)90033-8

Deepak Lal, Subhendu Som, Stanley Friedman

{"title":"Survival and mutagenic effects of 5-azacytidine in Escherichia coli","authors":"Deepak Lal, Subhendu Som, Stanley Friedman","doi":"10.1016/0167-8817(88)90033-8","DOIUrl":"10.1016/0167-8817(88)90033-8","url":null,"abstract":"<div>Survival and mutagenesis caused by 5-azacytidine was studied in Escherichia coli. Survival was partially lexA- and recA-dependent and was decreased by the presence of a DNA (cytosine-5)methyltransferase. The dcm, MspI, and EcoRII methyltransferase genes all decreased survival. There was no direct relationship between amount of methylase enzyme present and cell survival, but only plasmids containing a methylase gene sensitized cells to 5-azacytidine. Survival was not affected by uvrA, uvrB or umuCD mutations. Induction of sulA::lacZ fusions by 5-azacytidine was inhibited in strains containing elevated levels of DNA methylase. Cells resistant to 5-azacytidine when they contained a plasmid specifying the EcoRII methylase were sensitive if the plasmid specified the complete EcoRII restriction-modification system. The mechanism of cell death in these situations is therefore different.Mutation of the rpoB gene by 5-azacytidine was studied. The mutation rate was decreased by the presence of recA and lexA mutations. Mutation in umuCD had little effect on the mutation rate. The recA430 mutation, which does not support SOS-dependent mutagenesis induced by UV light, does support 5-azacytidine induced mutagenesis. The presence of DNA (cytosine-5)methyltransferase had no effect on the mutation rate caused by 5-azacytidine treatment.The mutagenic and lethal lesions caused by 5-azacytidine in the absence of methylase therefore differ from the lethal lesions that occur in the presence of methylase. The former could be due to the opening of the 5-azacytosine ring in DNA. Cell death in the presence of methylase could be due to tight binding of methylase to azacytosine containing DNA as well as inhibition of induction of the SOS response.</div>","PeriodicalId":100936,"journal":{"name":"Mutation Research/DNA Repair Reports","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"1988-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/0167-8817(88)90033-8","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"13598260","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 32

Damage-resistant DNA synthesis in Eukaryotes 真核生物抗损伤DNA合成

Mutation Research/DNA Repair Reports Pub Date : 1988-05-01 DOI: 10.1016/0167-8817(88)90030-2

Martin F. Lavin , Alice L. Schroeder

{"title":"Damage-resistant DNA synthesis in Eukaryotes","authors":"Martin F. Lavin , Alice L. Schroeder","doi":"10.1016/0167-8817(88)90030-2","DOIUrl":"10.1016/0167-8817(88)90030-2","url":null,"abstract":"<div>The molecular basis of sensitivity of ionizing radiation and other damaging agents is not clearly defined in eukaryotes. While a large number of mutants have been described only a few have been demonstrated to have a defect in the repair of damage to DNA. An interesting characteristic of a sub-group of these mutants, in different species extending throughout the phylogenetic scale, is the presence of damage-resistant DNA synthesis. This phenomenon is observed in cells from individuals with the genetic disorder ataxia telangiectasia, in HeLa cells treated with fluorodeoxyuridine prior to UV irradiation, in mutants of the fungus Neurospora crassa, the slime mould Dictyostelium discoideum, the fruit fly Drosophila melanogaster and possibly in the “wasted” mouse mutant. In the case of ataxia telangiectasia sensitivity is only observed to ionizing radiation or radiomimetic chemicals whereas sensitivity to a wider spectrum of mutagens is reported for the lower eukaryotic mutants. In all cases a reduced inhibition of DNA synthesis is obtained after exposure to an agent to which the cell type is hypersensitive. It is unclear how damage-resistant DNA synthesis contributes to increased sensitivity in these cells, but is unlikely to be the major mechanism predisposing to radiation-induced cell death. The description of a derivative of an ataxia telangiectasia cell line with normal sensitivity to radiation but still maintaining resistant DNA synthesis partially uncouples radioresistant DNA synthesis and radiosensitivity. This paper is designed to review the phenomenon of damage-resistant DNA synthesis in a number of mutants.</div>","PeriodicalId":100936,"journal":{"name":"Mutation Research/DNA Repair Reports","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"1988-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/0167-8817(88)90030-2","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"14100425","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 52

UV mutagenesis in E. coli with excision repair initiated by uvrABC or denV gene products 由uvrABC或denV基因产物引发的大肠杆菌切除修复的紫外线诱变

Mutation Research/DNA Repair Reports Pub Date : 1988-03-01 DOI: 10.1016/0167-8817(88)90039-9

R. Bockrath , M.Z. Hodes , P. Mosbaugh , K. Valerie , J.K. de Riel

{"title":"UV mutagenesis in E. coli with excision repair initiated by uvrABC or denV gene products","authors":"R. Bockrath , M.Z. Hodes , P. Mosbaugh , K. Valerie , J.K. de Riel","doi":"10.1016/0167-8817(88)90039-9","DOIUrl":"10.1016/0167-8817(88)90039-9","url":null,"abstract":"<div>Mutation frequency responses produced by ultraviolet light are compared in 4 closely related strains of E. coli B/r having the same tyr(Oc) allele and different excision-repair capabilities: uvr+ (excision repair initiated by wild-type UvrABC activity), uvrA (excision repair defective), uvrA/pdenV-7 (excision repair initiated by endonuclease V of bacteriophage T4, DenV activity), and uvr+/pdenV-7 (excision repair initiated by UvrABC and DenV activities). The production of Tyr+ prototrophic mutants is classified into back-mutations and de novo or converted glutamine tRNA suppressor mutations to indicate different mutation events. Cells transformed with the plasmid pdenV-7 require larger exposures than the parent strains to produce comparible mutation frequency responses, indicating that DenV activity can repair mutagenic photoproducts. When damage reduction by UvrABC or DenV is compared for each of the specific categories of mutation, the results are consistent with the idea that pyrimidine dimers infrequently or never target back-mutations of this allele, frequently target the de novo suppressor mutations, and extensively or exclusively target the converted suppressor mutations. This analysis is based on the distinction that UvrABC-initiated excision repair recognizes dimer and non-dimer (pyrimidine (4–6) pyrimidone) photoproducts but that DenV-initiated repair recognizes only pyrimidine dimers.</div>","PeriodicalId":100936,"journal":{"name":"Mutation Research/DNA Repair Reports","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"1988-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/0167-8817(88)90039-9","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"14408866","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 6

A Chinese hamster ovary cell line hypersensitive to ionizing radiation and deficient in repair replication 中国仓鼠卵巢细胞系对电离辐射超敏感和修复复制缺陷

Mutation Research/DNA Repair Reports Pub Date : 1988-03-01 DOI: 10.1016/0167-8817(88)90041-7

Lloyd F. Fuller, Robert B. Painter

{"title":"A Chinese hamster ovary cell line hypersensitive to ionizing radiation and deficient in repair replication","authors":"Lloyd F. Fuller, Robert B. Painter","doi":"10.1016/0167-8817(88)90041-7","DOIUrl":"10.1016/0167-8817(88)90041-7","url":null,"abstract":"<div>An X-ray-sensitive Chinese hamster ovary cell line was isolated by means of a semi-automated procedure in which mutagenized cells formed colonies on top of agar, were X-irradiated, and were photographed at two later times. We compared the photographs to identify colonies that displayed significant growth arrest. One of the colonies identified in this manner produced a stable line (irs1SF) that is hypersensitive to ionizing radiation. The X-ray dose at which 10% of the population survives (D10) is 2.25 Gy for irs1SF and 5.45 Gy for the parental line. The new mutant is also moderately sensitive to ethyl methanesulfonate. irs1SF performs only half as much X-ray-induced repair replication as the parental line, indicating a defect in excision repair. This defect is believed to be the primary cause of the line's radiosensitivity. Although irs1SF repairs DNA double-strand breaks at a normal rate, it repairs single-strand breaks more slowly than normal. irs1SF has an elevated number of spontaneous chromatid aberrations and produces significantly higher numbers of X-ray-induced chromatid aberrations after exposure during the G1 phase of the cell cycle. The line is hypomutable, with X-ray exposure inducing only one-third as many 6-thioguanine-resistant colonies as the parental line.</div>","PeriodicalId":100936,"journal":{"name":"Mutation Research/DNA Repair Reports","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"1988-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/0167-8817(88)90041-7","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"14473276","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 185