大肠杆菌一种特定外膜脂蛋白的嘌呤霉素抗性生物合成。
Puromycin-resistant biosynthesis of a specific outer-membrane lipoprotein of Escherichia coli.
作者信息
Halegoua S, Hirashima A, Inouye M
出版信息
J Bacteriol. 1976 Apr;126(1):183-91. doi: 10.1128/jb.126.1.183-191.1976.
Abstract
The reported puromycin resistance of the in vivo biosynthesis of a specific outer-membrane lipoprotein of Escherichia coli was further investigated. The biosynthetic machinery making the lipoprotein was made more accessible to puromycin by disruption of the cell structure using ethylenediaminetetracetate or toluene, and finally in an in vitro protein biosynthesis system using polyribosomes. Puromycin sensitivity of overall protein synthesis increased by about 10-fold for each method of disruption of the cell structure; 50% inhibitions were obtained at 330, 35, 2.7, and 0.22 mug of puromycin per ml for intact cells, ethylenediaminetetraacetate-treated cells, toluene-treated cells, and the polyribosome system, respectively. However, the lipoprotein biosynthesis remained more resistant to puromycin than the biosynthesis of other proteins in all systems tested. These results strongly suggest that puromycin resistance of the lipoprotein biosynthesis is due to an intrinsic property of the lipoprotein biosynthetic machinery.
摘要
对大肠杆菌特定外膜脂蛋白体内生物合成中所报道的嘌呤霉素抗性进行了进一步研究。通过使用乙二胺四乙酸或甲苯破坏细胞结构，使合成脂蛋白的生物合成机制对嘌呤霉素更易接近，最终在使用多核糖体的体外蛋白质生物合成系统中也是如此。对于每种破坏细胞结构的方法，总体蛋白质合成对嘌呤霉素的敏感性增加了约10倍；完整细胞、乙二胺四乙酸处理的细胞、甲苯处理的细胞和多核糖体系统分别在每毫升330、35、2.7和0.22微克嘌呤霉素时获得50%的抑制率。然而，在所有测试系统中，脂蛋白生物合成对嘌呤霉素的抗性仍高于其他蛋白质的生物合成。这些结果有力地表明，脂蛋白生物合成对嘌呤霉素的抗性是由于脂蛋白生物合成机制的内在特性。
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