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大肠杆菌中冷敏感型sec突变的多拷贝抑制

Multicopy suppression of cold-sensitive sec mutations in Escherichia coli.

作者信息

Danese P N, Murphy C K, Silhavy T J

机构信息

Department of Molecular Biology, Princeton University, New Jersey 08544-1014, USA.

出版信息

J Bacteriol. 1995 Sep;177(17):4969-73. doi: 10.1128/jb.177.17.4969-4973.1995.

Abstract

Mutations in the secretory (sec) genes in Escherichia coli compromise protein translocation across the inner membrane and often confer conditional-lethal phenotypes. We have found that overproduction of the chaperonins GroES and GroEL from a multicopy plasmid suppresses a wide array of cold-sensitive sec mutations in E. coli. Suppression is accompanied by a stimulation of precursor protein translocation. This multicopy suppression does not bypass the Sec pathway because a deletion of secE is not suppressed under these conditions. Surprisingly, progressive deletion of the groE operon does not completely abolish the ability to suppress, indicating that the multicopy suppression of cold-sensitive sec mutations is not dependent on a functional groE operon. Indeed, overproduction of proteins unrelated to the process of protein export suppresses the secE501 cold-sensitive mutation, suggesting that protein overproduction, in and of itself, can confer mutations which compromise protein synthesis and the observation that low levels of protein synthesis inhibitors can suppress as well. In all cases, the mechanism of suppression is unrelated to the process of protein export. We suggest that the multicopy plasmids also suppress the sec mutations by compromising protein synthesis.

摘要

大肠杆菌中分泌(sec)基因的突变会损害蛋白质跨内膜的转运,并常常导致条件致死表型。我们发现,从多拷贝质粒过量表达伴侣蛋白GroES和GroEL可抑制大肠杆菌中一系列广泛的冷敏感sec突变。抑制伴随着前体蛋白转运的刺激。这种多拷贝抑制并不绕过Sec途径,因为在这些条件下secE的缺失不会被抑制。令人惊讶的是,groE操纵子的逐步缺失并没有完全消除抑制能力,这表明对冷敏感sec突变的多拷贝抑制并不依赖于功能性的groE操纵子。实际上,过量表达与蛋白质输出过程无关的蛋白质可抑制secE501冷敏感突变,这表明蛋白质的过量表达本身就可以导致损害蛋白质合成的突变,而且低水平的蛋白质合成抑制剂也能起到抑制作用。在所有情况下,抑制机制都与蛋白质输出过程无关。我们认为,多拷贝质粒也通过损害蛋白质合成来抑制sec突变。

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