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大肠杆菌tufA缺陷菌株中的生长速率、核糖体合成及延伸因子合成

Rates of growth, ribosome synthesis and elongation factor synthesis in a tufA defective strain of E. coli.

作者信息

Gausing K

出版信息

Mol Gen Genet. 1981;184(2):272-7. doi: 10.1007/BF00272916.

Abstract

A tufA defective strain of E. coli was isolated which by a single deletion event acquired a tufA-lacZ fusion gene and lost the normal functional tufA gene (see accompanying paper). A correlation between the growth rate of protein synthesis was decreased to about 50% in the tufA defective strain whereas the number of EF-Tu molecules per ribosome was about 80% compared to a normal strain. The results indicate that tufB gene expression was preferentially stimulated in the tufA defective strain but the increased EF-TuB synthesis was not sufficient to make up for the loss of normal EF-TuA synthesis. Introduction of a plasmid that carries a complete tufA gene and the preceeding fusA gene but not the str-promotor into the tufA defective strain did not alleviate the slow growth or low rate of EF-Tu synthesis showing that the high rate of EF-TuA synthesis compared to the other proteins in the str operon is not augmented by a strong second promotor for the tufA gene. The tufA-lacZ fusion which takes the place of the normal tufA gene was expressed at a high rate and the beta-galactosidase activity increased with the growth rate as expected.

摘要

分离出一株大肠杆菌的tufA缺陷菌株,该菌株通过一次缺失事件获得了一个tufA - lacZ融合基因,并失去了正常功能的tufA基因(见随附论文)。在tufA缺陷菌株中,蛋白质合成的生长速率相关性降低至约50%,而与正常菌株相比,每个核糖体的EF - Tu分子数量约为80%。结果表明,tufB基因表达在tufA缺陷菌株中受到优先刺激,但增加的EF - TuB合成不足以弥补正常EF - TuA合成的损失。将携带完整tufA基因和前导fusA基因但不含str启动子的质粒导入tufA缺陷菌株,并未缓解其生长缓慢或EF - Tu合成速率低的问题,这表明与str操纵子中的其他蛋白质相比,tufA基因的高EF - TuA合成速率并未因tufA基因的强第二个启动子而增加。取代正常tufA基因的tufA - lacZ融合基因以高速率表达,并且β - 半乳糖苷酶活性如预期的那样随生长速率增加。

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