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Tn5介导的大肠杆菌博来霉素抗性需要宿主基因的表达。

Tn5-mediated bleomycin resistance in Escherichia coli requires the expression of host genes.

作者信息

Blot M, Heitman J, Arber W

机构信息

Abteilung Mikrobiologie, Universität Basel, Switzerland.

出版信息

Mol Microbiol. 1993 Jun;8(6):1017-24. doi: 10.1111/j.1365-2958.1993.tb01646.x.

Abstract

The transposon Tn5 expresses a gene, ble, whose product increases the viability of Escherichia coli and also confers resistance to the DNA-cleaving antibiotic bleomycin and the DNA-alkylating agent ethylmethanesulphonate. We find that the Ble protein induces expression of an alkylation inducible gene, aidC, and that both the AidC gene product and DNA polymerase I are required for Ble to confer bleomycin resistance. These findings support models in which Ble enhances DNA repair and suggest that Tn5 confers a fitness advantage to the host bacterium by increasing the repair of spontaneous DNA lesions. Such co-operation between a transposon and its host suggests that Tn5 is a symbiotic rather than a selfish DNA element.

摘要

转座子Tn5表达一个基因ble,其产物可提高大肠杆菌的生存能力,还能赋予对DNA切割抗生素博来霉素和DNA烷化剂甲磺酸乙酯的抗性。我们发现Ble蛋白诱导一个烷基化诱导基因aidC的表达,并且Ble赋予博来霉素抗性需要AidC基因产物和DNA聚合酶I。这些发现支持了Ble增强DNA修复的模型,并表明Tn5通过增加对自发DNA损伤的修复赋予宿主细菌适应性优势。转座子与其宿主之间的这种合作表明Tn5是一种共生而非自私的DNA元件。

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