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磷酸盐缓冲琼脂对大肠杆菌菌株中紫外线诱导的链霉素抗性突变数量的影响。

Effect of phosphate buffer agar on the number of UV-induced mutations to streptomycin resistance in Escherichia coli strains.

作者信息

Specht S M, Sideropoulos A S

机构信息

Department of Biological Sciences, Duquesne University, Pittsburgh, Pennsylvania 15282.

出版信息

Microbios. 1990;62(252-253):187-95.

PMID:2195304
Abstract

The number of UV-induced mutations to streptomycin resistance in Escherichia coli B/r cells depends on the post-irradiation incubation medium. When cells are incubated on phosphate buffer agar (PBA) as opposed to brain heart infusion agar (BHI), there is an irreversible loss in the number of potential streptomycin resistant mutants which develop. This decrease in mutant numbers is known to occur without a corresponding loss in overall cell viability and cannot be explained in terms of the kinetics of dimer excision. Recent studies have indicated that pyrimidine dimers are the substrate for this repair on PBA. The genetics of PBA repair was investigated by observing the influence of the post-irradiation incubation medium (PBA vs BHI) on the number of streptomycin resistant mutants which develop in E. coli strains deficient in various repair pathways. A recB and recC strain (WP3 recB trp-; WP7 recC trp-) showed repair of potential streptomycin resistant mutants similar to that of B/r when incubated on PBA following irradiation. The medium had no effect on the number of mutants expressed in an excision deficient uvrA- strain (WP2 uvrA trp-) or a polymerase I mutant (P3478 polA thy-). This was interpreted to mean that the loss of streptomycin resistant mutants on PBA involves the excision repair pathway and is dependent on the polA gene product, polymerase I.

摘要

大肠杆菌B/r细胞中紫外线诱导的对链霉素抗性的突变数量取决于照射后的培养介质。与脑心浸液琼脂(BHI)相比,当细胞在磷酸盐缓冲琼脂(PBA)上培养时,产生的潜在链霉素抗性突变体数量会出现不可逆的减少。已知这种突变体数量的减少在总体细胞活力没有相应损失的情况下发生,并且无法用二聚体切除动力学来解释。最近的研究表明,嘧啶二聚体是PBA上这种修复的底物。通过观察照射后的培养介质(PBA与BHI)对缺乏各种修复途径的大肠杆菌菌株中产生的链霉素抗性突变体数量的影响,研究了PBA修复的遗传学。recB和recC菌株(WP3 recB trp-;WP7 recC trp-)在照射后在PBA上培养时,显示出与B/r类似的潜在链霉素抗性突变体的修复。该培养基对切除缺陷的uvrA-菌株(WP2 uvrA trp-)或聚合酶I突变体(P3478 polA thy-)中表达的突变体数量没有影响。这被解释为意味着PBA上链霉素抗性突变体的减少涉及切除修复途径,并且依赖于polA基因产物聚合酶I。

相似文献

1
Effect of phosphate buffer agar on the number of UV-induced mutations to streptomycin resistance in Escherichia coli strains.磷酸盐缓冲琼脂对大肠杆菌菌株中紫外线诱导的链霉素抗性突变数量的影响。
Microbios. 1990;62(252-253):187-95.
2
The effect of streptomycin resistance, caffeine and acriflavine on ultraviolet light-induced reversion to tryptophan independence in strains of Escherichia coli B/r.链霉素抗性、咖啡因和吖啶黄对大肠杆菌B/r菌株中紫外线诱导回复为色氨酸非依赖型的影响。
Mutat Res. 1975 Nov;30(2):163-76.
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[Radioadaptive enhancement of the repair of UV-induced postreplication gaps in Escherichia coli cells deficient in DNA repair].[DNA修复缺陷的大肠杆菌细胞中紫外线诱导的复制后间隙修复的辐射适应性增强]
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Role of pyrimidine dimer excision in loss of potential streptomycin resistance mutations of ultraviolet-irradiated Escherichia coli on phosphate-buffered agar.嘧啶二聚体切除在磷酸盐缓冲琼脂上紫外线照射的大肠杆菌潜在链霉素抗性突变丧失中的作用
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Elevated mutability of polA derivatives of Escherichia coli B/r at sublethal doses of ultraviolet light: evidence for an inducible error-prone repair system ("SOS repair") and its anomalous expression in these strains.大肠杆菌B/r的polA衍生物在亚致死剂量紫外线照射下的突变率升高:诱导性易错修复系统(“SOS修复”)的证据及其在这些菌株中的异常表达。
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[Participation of the product of gene dnaG in the slow nonmutagenic repair pathway for gamma-induced single-stranded DNA breaks in Escherichia coli cells].[基因dnaG的产物参与大肠杆菌细胞中γ射线诱导的单链DNA断裂的缓慢非诱变修复途径]
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Mistranslation and genetic variability: the effect of streptomycin.错译与基因变异性:链霉素的作用
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Are there two mechanisms of induction by ultraviolet light of streptomycin-resistant mutations in Escherichia coli?紫外线诱导大肠杆菌链霉素抗性突变是否存在两种机制?
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Repair of UV-irradiated plasmid DNA in mutants of Saccharomyces cerevisiae and Escherichia coli deficient in repair of pyrimidine dimers.酿酒酵母和大肠杆菌嘧啶二聚体修复缺陷突变体中紫外线照射质粒DNA的修复
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[Increase in the fraction of non-repaired mutations in Escherichia coli cells, incubated in the absence of glucose after UV-irradiation].[紫外线照射后在无葡萄糖条件下培养的大肠杆菌细胞中未修复突变比例的增加]
Genetika. 1990 Sep;26(9):1679-81.

引用本文的文献

1
Mutation frequency decline in Escherichia coli. II. Kinetics support the involvement of transcription-coupled excision repair.大肠杆菌中的突变频率下降。II. 动力学支持转录偶联切除修复的参与。
Mol Gen Genet. 1995 Dec 20;249(6):591-9. doi: 10.1007/BF00418028.