Mutation Research/DNA Repair Reports最新文献_第2页

Complementation of the DNA-repair defect in a CHO mutant by human DNA that lacks highly abundant repetitive sequences 缺乏高度丰富重复序列的人DNA对CHO突变体中DNA修复缺陷的补充

Mutation Research/DNA Repair Reports Pub Date : 1988-11-01 DOI: 10.1016/0167-8817(88)90022-3

Ann M. Dulhanty , Jaime S. Rubin , Gordon F. Whitmore

{"title":"Complementation of the DNA-repair defect in a CHO mutant by human DNA that lacks highly abundant repetitive sequences","authors":"Ann M. Dulhanty , Jaime S. Rubin , Gordon F. Whitmore","doi":"10.1016/0167-8817(88)90022-3","DOIUrl":"10.1016/0167-8817(88)90022-3","url":null,"abstract":"<div>Recently, two human DNA-repair genes have been cloned which complement the defects in complementation groups 1 and 2 of the CHO mutants which are sensitive to ultraviolet light and deficient in the incision step of excision repair. Here we report human gene transfer-mediated complementation of a group 4 CHO mutant sensitive to ultraviolet light and mitomycin C (MMC). The transfectants generated by transfecting human DNA into the repair-deficient cell line demonstrate the repair-proficient phenotype, as they have wild-type levels of resistance to UV light and MMC and are competent in performing the incision step of excision erpair in response to UV irradiation. 3 of the 8 transfectants isolated display no detectable human repetitive sequences, while the other 5 contain varying amounts of human repetitive DNA. As the evidence suggests that all of the transfectants are repair-proficient as a result of the uptake of humand DNA, we conclude that the human gene that complements the repair defect in group 4 CHO mutants contains no highly abundant human repetitive sequences. This imposes the necessity of developing cloning strategies involving the identification of sequences that flank the gene.</div>","PeriodicalId":100936,"journal":{"name":"Mutation Research/DNA Repair Reports","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"1988-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/0167-8817(88)90022-3","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"14273151","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: 12

Excision repair of pyrimidine dimers in human peripheral blood lymphocytes: Comparison between mitogen stimulated and unstimulated cells 人外周血淋巴细胞嘧啶二聚体的切除修复:有丝分裂原刺激与未刺激细胞的比较

Mutation Research/DNA Repair Reports Pub Date : 1988-09-01 DOI: 10.1016/0167-8817(88)90016-8

Steven E. Freeman, Sharon L. Ryan

引用次数: 31

The induction of rho− mutants by UV or γ-rays is independent of the nuclear recombinational repair pathway in Saccharomyces cerevisiae 在酿酒酵母中，紫外线或γ射线诱导的rho -突变体与核重组修复途径无关

Mutation Research/DNA Repair Reports Pub Date : 1988-09-01 DOI: 10.1016/0167-8817(88)90017-X

Martine Heude

引用次数: 3

A mutation in the DNA adenine methylase gene (dam) of Salmonella typhimurium decrease susceptibility to 9-aminoacridine-induced frameshift mutagenesis 鼠伤寒沙门菌DNA腺嘌呤甲基化酶基因(dam)突变降低了对9-氨基吖啶诱导的移码突变的易感性

Mutation Research/DNA Repair Reports Pub Date : 1988-09-01 DOI: 10.1016/0167-8817(88)90015-6

Lyndal Ritchie, Denis M. Podger, Ruth M. Hall

{"title":"A mutation in the DNA adenine methylase gene (dam) of Salmonella typhimurium decrease susceptibility to 9-aminoacridine-induced frameshift mutagenesis","authors":"Lyndal Ritchie, Denis M. Podger, Ruth M. Hall","doi":"10.1016/0167-8817(88)90015-6","DOIUrl":"10.1016/0167-8817(88)90015-6","url":null,"abstract":"<div>A mutant of Salmonella typhimurium with a reduced response to mutation induction by 9-aminoacridine (9AA) has been isolated. The mutation (dam-2) is located in the DNA adenine methylase gene. The dam-2 mutant strain exhibits a level of sensitivity to 2-aminopourine(2AP) intermediate between that of the dam+ and the DNA adenine methylation-decifit dam-1 strain, and 2AP sensitivity was reversed by introduction of a muH mutation or the plasmid pMQ148 (which carries a functional Escherichia coli dam+ gene). However, the dam-2 strain is not grossly defective in DNA adenine methylase activity. Whole cell DNA appears full methylated at -GATC- sites.The levels of 9AA required to induced equivalent levels of frameshift mutagnesis in the dam-2 strain were approximately 2-fold higher than for the dam+ strain. Introduction of pMQ148 dam+ reduced the level of 9AA required for induction of frameshift mutations 4-fold in the dam-2 strain and 2-fold in the dam+ strain. The dam-2 mutation had no effect on the levels of ICR191 required for induction of frameshift mutation, but introduction of pMQ148 reduced the ICR191-induced mutagenesis 2-fold. The dam+ / pMQ148, dam-2/ pMQ148 and dam-1 / pMQ148 strains showed identical dose-receptor identical dose-response curves for both 9AA and ICR191. These results are consistent with a slightly reduced )(dam-2) or increased (PmQ148) rate of methylation at the replication fork.The 2AP sensitivity of the dam-2 strain cannot be simply explained. Futhermore, addition of methione to the assay medium reverses the 2AP sensitivity of the dam-2 strain, but has no effect on 9AA mutaganesis.</div>","PeriodicalId":100936,"journal":{"name":"Mutation Research/DNA Repair Reports","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"1988-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/0167-8817(88)90015-6","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"13979217","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: 2

Detection of DNA damage and repair by alkaline elution using human lymphocytes 人淋巴细胞碱性洗脱法检测DNA损伤及修复

Mutation Research/DNA Repair Reports Pub Date : 1988-09-01 DOI: 10.1016/0167-8817(88)90012-0

J.S. Munzer, S.K. Jones, J.P. O'Neill, J.N. Hartshorn, S.H. Robison

引用次数: 7

Identification of a new seventh complementation group of UV-sensitive mutants in Chinese hamster cells 中国仓鼠细胞第7个新的紫外敏感突变体互补群的鉴定

Mutation Research/DNA Repair Reports Pub Date : 1988-09-01 DOI: 10.1016/0167-8817(88)90018-1

Małgorzata Z. Zdzienicka , G.P. van der Schans , J.W.I.M. Simons

引用次数: 34

Repair of DNA single-strand and double-strand breaks in the Chinese hamster xrs 5 mutant cell line as determined by DNA unwinding 中国仓鼠xrs5突变细胞系DNA单链和双链断裂的DNA解绕修复

Mutation Research/DNA Repair Reports Pub Date : 1988-09-01 DOI: 10.1016/0167-8817(88)90011-9

Nina D. Costa, Peter E. Bryant

引用次数: 32

SOS independent survival against mitomycin C induced lethality in a rifampicin-nalidixic acid-resistant mutant of Escherichia coli 抗丝裂霉素C的SOS独立存活诱导大肠埃希菌抗利福平-萘啶酸突变体致死

Mutation Research/DNA Repair Reports Pub Date : 1988-09-01 DOI: 10.1016/0167-8817(88)90013-2

K.R. Kumaresan, R. Jayaraman

{"title":"SOS independent survival against mitomycin C induced lethality in a rifampicin-nalidixic acid-resistant mutant of Escherichia coli","authors":"K.R. Kumaresan, R. Jayaraman","doi":"10.1016/0167-8817(88)90013-2","DOIUrl":"10.1016/0167-8817(88)90013-2","url":null,"abstract":"<div>A combination of specific rifampicin-resistant (rpo B87) and nalidixic acid-resistant (gyrA87) mutations results in a marked increase in the survival of Escherichia coli against mitomycin C-induced lethality in mutants defective for SOS induction and excision repair. Although the response does not seem to be obligatorily dependent upon the RecA protein, the efficiency is markedly increased in its presence, even in a conventionally inactive form. This response is not elicited against lethality due to ultraviolet radiation or N-methyl-N′-nitro-N-nitrosoguanidine exposure. The combination of rpo B87 and gyrA87 mutations also greatly alleviates post-mitomycin C degradation of DNA under SOS non-inducible conditions. It is proposed that the rpo B subunit of RNA polymerase and gyrA subunit of DNA gyrase could participate in the repair of certain types of DNA damage, such as cross-links, in a mode independent of SOS-regulated excision repair and post-replication repair.</div>","PeriodicalId":100936,"journal":{"name":"Mutation Research/DNA Repair Reports","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"1988-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/0167-8817(88)90013-2","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"14178306","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: 8

Radiation-induced recovery processes in cultured marsupial cells 辐射诱导培养有袋动物细胞的恢复过程

Mutation Research/DNA Repair Reports Pub Date : 1988-09-01 DOI: 10.1016/0167-8817(88)90010-7

Ronald Overberg , Gamini Chandrasena, Claud S. Rupert

{"title":"Radiation-induced recovery processes in cultured marsupial cells","authors":"Ronald Overberg , Gamini Chandrasena, Claud S. Rupert","doi":"10.1016/0167-8817(88)90010-7","DOIUrl":"10.1016/0167-8817(88)90010-7","url":null,"abstract":"<div>The ultraviolet sensitivity of Potorous tridactylus male kidney (PtK-2) cells is markedly increased by post irradiation treatment for 24 h with 5 μM emetime (which inhibits protein synthesis by acting on the 40S ribosomal subunit), or with 5 μM cycloheximide (which inhibits by interaction with the 60S subunit), or with the RNA polymerase II inhibitor 5,6,-dichloro-1-ß-ribofuranosylbenzimidazole at 50 μM. All 3 treatments give the same sensitivity, while unirradiated cells are little affected. Shortening the time of treatment, or delaying application of the drugs decreases their effect on the same time schedule. Preirradiation of cells, with no drug treatment in the following 8 h, diminishes the sensitivity to a subsequent irradiation with protein synthesis blocked afterwards. Photoreactivation immediately following such preirradiation eliminates its desensitizing effect. Inhibiting protein synthesis after irradiation also markedly reduces the frequency of UV-induced mutants in the surviving population. These facts suggest that gene expression in the period following irradiation facilitates recovery from radiation damage, with an increased probability of mutation, reminiscent of the “SOS response” in Escherichia coli.</div>","PeriodicalId":100936,"journal":{"name":"Mutation Research/DNA Repair Reports","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"1988-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/0167-8817(88)90010-7","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"14537815","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 responses of mitomycin C-sensitive mouse lymphoma cell mutants to other DNA cross-linking agents 丝裂霉素c敏感小鼠淋巴瘤细胞突变体对其他DNA交联剂的生存和致突变反应

Mutation Research/DNA Repair Reports Pub Date : 1988-09-01 DOI: 10.1016/0167-8817(88)90014-4

Hiroko Hama-Inaba , Koki Sato , Ethel Moustachhi

{"title":"Survival and mutagenic responses of mitomycin C-sensitive mouse lymphoma cell mutants to other DNA cross-linking agents","authors":"Hiroko Hama-Inaba , Koki Sato , Ethel Moustachhi","doi":"10.1016/0167-8817(88)90014-4","DOIUrl":"10.1016/0167-8817(88)90014-4","url":null,"abstract":"<div>Mitomycin C-sensitive mutants MCN 151 (complementation group I) and MCE 50 (complementation group II) derived from mouse lymphoma L5178Y cells were found to be also highly sensitive to the lethal effects of other DNA cross-linking agents, such as photoaddition of 8-methoxypsoralen (8-MOP) and cis-diamminedichloroplatinum II (cis-DDP). They were less sensitive to the monofunctional derivative 3-carbethoxypsoralen (3-CPs) and to trans-DDP than their bifunctional counterparts.Incorporation levels of labeled 8-MOP or 3-CPs in wild-type cells and 2 mutants were almost the same, indicating that the sensitivity is not caused by differential incorporation of the agents.The rates of photoinduced mutations to 6-thioguanine resistance in the mutants, per unit dose of 8-MOP, were about 4 times higher for MNC 151 and 3 times higher for MCE 506 than that in L5178Y cells. However, the rates of induced mutations per viable cells in the mutants were nearly equal to those in wild-type cells.Cross-link repair was compared between mutants and wild-type cells by using the alkaline sucrose-gradient gradient sedimentation technique. The results show that normal cells and both mutants are able to incise the cross-linked DNA, which is the fisrst step of cross-link repair.</div>","PeriodicalId":100936,"journal":{"name":"Mutation Research/DNA Repair Reports","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"1988-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/0167-8817(88)90014-4","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"14537812","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: 14