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核糖体降解在饥饿大肠杆菌细胞死亡中的作用。

Role of ribosome degradation in the death of starved Escherichia coli cells.

作者信息

Davis B D, Luger S M, Tai P C

出版信息

J Bacteriol. 1986 May;166(2):439-45. doi: 10.1128/jb.166.2.439-445.1986.

Abstract

In Escherichia coli cultures limited for phosphate, the number of ribosomal particles was reduced to a small percentage of its earlier peak value by the time the viable cell count began to drop; the 30S subunits decreased more than the 50S subunits. Moreover, the ribosomal activity was reduced even more: these cells no longer synthesized protein, and their extracts could not translate phage RNA unless ribosomes were added. The translation initiation factors also disappeared, suggesting that they become less stable when released from their normal attachment to 30S subunits. In contrast, elongation factors, aminoacyl-tRNA synthetases, and tRNA persisted. During further incubation, until viability was reduced to 10(-5), the ribosomal particles disappeared altogether, while tRNA continued to be preserved. These results suggest that an excessive loss of ribosomes (and of initiation factors) may be a major cause of cell death during prolonged phosphate starvation.

摘要

在磷受限的大肠杆菌培养物中,到活菌数开始下降时,核糖体颗粒的数量降至其早期峰值的一小部分;30S亚基的减少比50S亚基更多。此外,核糖体活性降低得更多:这些细胞不再合成蛋白质,并且其提取物除非添加核糖体否则无法翻译噬菌体RNA。翻译起始因子也消失了,这表明它们从与30S亚基的正常附着中释放出来时变得不太稳定。相比之下,延伸因子、氨酰-tRNA合成酶和tRNA持续存在。在进一步孵育期间,直到活力降至10^(-5),核糖体颗粒完全消失,而tRNA继续保留。这些结果表明,核糖体(和起始因子)的过度损失可能是长期磷饥饿期间细胞死亡的主要原因。

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