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在用N-甲基-N'-硝基-N-亚硝基胍处理后,大肠杆菌RecA蛋白在酿酒酵母修复缺陷型pso4-1和rad51::URA3突变体中表达的生物学后果。

Biological consequences of E.coli RecA protein expression in the repair defective pso4-1 and rad51::URA3 mutants of S. cerevisiae after treatment with N-methyl-N'-nitro-N-nitrosoguanidine.

作者信息

Slaninová M, Vlcková V, Brozmanová J, Morais M A, Henriques J A

机构信息

Department of Genetics, Faculty of Natural Sciences, Comenius University, Bratislava, Slovakia.

出版信息

Neoplasma. 1996;43(5):315-9.

PMID:8996551
Abstract

RecA protein of E.coli is a multifunctional protein participating in genetic recombination, recombinational repair and mutagenesis. We used E.coli recA gene as a probe for complementation of repair defects after treatment of N-methyl-N'-nitro-N-nitrosoguanidine in the pso4-1 and rad51::URA3 mutants of S. cerevisiae. We tried to find the role of the RecA protein in S. cerevisiae mutants defective in different repair pathways. The RecA protein had no effect on survival of haploid and diploid pso4-1 mutants, but it had a significant effect on MNNG induced mutagenesis, which was increased to the wild type level. No effect of the RecA protein on survival was observed in rad51::URA3 mutant after MNNG treatment. However, in this case the RecA protein decreased the induced mutagenesis. We can suppose that the RecA protein, with its multifunctional enzymatic activity, can bind to special intermediates and initiate function of different repair pathways depending on repair defects of the mutants studied.

摘要

大肠杆菌的RecA蛋白是一种多功能蛋白,参与基因重组、重组修复和诱变。我们使用大肠杆菌recA基因作为探针,用于在酿酒酵母的pso4-1和rad51::URA3突变体中经N-甲基-N'-硝基-N-亚硝基胍处理后修复缺陷的互补实验。我们试图找出RecA蛋白在不同修复途径存在缺陷的酿酒酵母突变体中的作用。RecA蛋白对单倍体和二倍体pso4-1突变体的存活没有影响,但对MNNG诱导的诱变有显著影响,诱变率增加到野生型水平。在MNNG处理后,未观察到RecA蛋白对rad51::URA3突变体存活的影响。然而,在这种情况下,RecA蛋白降低了诱导的诱变率。我们可以推测,具有多功能酶活性的RecA蛋白可以结合特殊中间体,并根据所研究突变体的修复缺陷启动不同修复途径的功能。

相似文献

1
Biological consequences of E.coli RecA protein expression in the repair defective pso4-1 and rad51::URA3 mutants of S. cerevisiae after treatment with N-methyl-N'-nitro-N-nitrosoguanidine.在用N-甲基-N'-硝基-N-亚硝基胍处理后,大肠杆菌RecA蛋白在酿酒酵母修复缺陷型pso4-1和rad51::URA3突变体中表达的生物学后果。
Neoplasma. 1996;43(5):315-9.
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Defects in base excision repair combined with elevated intracellular dCTP levels dramatically reduce mutation induction in yeast by ethyl methanesulfonate and N-methyl-N'-nitro-N-nitrosoguanidine.碱基切除修复缺陷与细胞内dCTP水平升高相结合,可显著降低甲磺酸乙酯和N-甲基-N'-硝基-N-亚硝基胍对酵母的诱变作用。
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[Inactivating effect of N-methyl-N'-nitro-N-nitrosoguanidine on yeasts with different ploidies].[N-甲基-N'-硝基-N-亚硝基胍对不同倍性酵母的灭活作用]
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Further phenotypic characterization of pso mutants of Saccharomyces cerevisiae with respect to DNA repair and response to oxidative stress.酿酒酵母pso突变体在DNA修复及对氧化应激反应方面的进一步表型特征分析。
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Saturation mutagenesis of the E. coli RecA loop L2 homologous DNA pairing region reveals residues essential for recombination and recombinational repair.大肠杆菌RecA环L2同源DNA配对区域的饱和诱变揭示了重组和重组修复所必需的残基。
J Mol Biol. 1999 Mar 5;286(4):1097-106. doi: 10.1006/jmbi.1998.2515.

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How heterologously expressed Escherichia coli genes contribute to understanding DNA repair processes in Saccharomyces cerevisiae.异源表达的大肠杆菌基因如何有助于理解酿酒酵母中的DNA修复过程。
Curr Genet. 2004 Dec;46(6):317-30. doi: 10.1007/s00294-004-0536-2. Epub 2004 Nov 13.