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首页> 外文期刊>Genes & Genetic Systems >Suppression by enhanced RpoE activity of the temperature-sensitive phenotype of a degP ssrA double mutant in Escherichia coli
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Suppression by enhanced RpoE activity of the temperature-sensitive phenotype of a degP ssrA double mutant in Escherichia coli

机译：通过增强RpoE活性抑制大肠杆菌中degP ssrA双突变体的温度敏感性表型

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摘要

SsrA is a small RNA playing a crucial role in trans-translation, which leads to rescue of stalled ribosomes on or at the end of mRNA and addition of the degradation tag to a growing polypeptide. The lack of SsrA has been shown to enhance the temperature-sensitive (ts) phenotype of an E. coli strain defective in the degP gene, which encodes one of the periplasmic proteases. This severe ts phenotype was relieved only partially by an SsrA super(DD) variant, which can lead to ribosome rescue but adds a protease-resistant tag instead of the degradation tag, suggesting that accumulation of polypeptides programmed by truncated mRNAs is responsible for growth defect of the ssrA degP mutant. Expression of an S210A-mutant DegP protein, which lacks the protease activity but retains the chaperone activity, could relieve the ts phenotype of the double mutant, suggesting that the chaperone activity but not the protease activity of DegP is required for growth of the ssrA- deficient cells at high temperature. Overexpression of the rpoE gene, which encodes 蟽 super(E) responsible for the expression of factors involved in extracellular stress response, also suppressed the ts phenotype of the ssrA degP mutant. This suggests that the stress-responsing pathway(s) may be involved in the enhancement of ts phenotype of degP mutant in the absence of SsrA.
机译：SsrA是一种小RNA，在反式翻译中起着至关重要的作用，这可以挽救停滞的核糖体在mRNA或mRNA的末端，并将降解标签添加到生长中的多肽上。 SsrA的缺乏已显示出可增强degP基因缺陷的大肠杆菌菌株的温度敏感性（ts）表型，该菌株编码一种周质蛋白酶。这种严重的ts表型只能通过SsrA super（DD）变体部分缓解，这可以导致核糖体抢救，但增加了蛋白酶抗性标签而不是降解标签，表明由截短的mRNA编程的多肽积累是造成生长缺陷的原因的ssrA degP突变体。 S210A突变的DegP蛋白的表达缺乏蛋白酶活性，但保留了伴侣活性，可以缓解双重突变体的ts表型，这表明ssrA-的生长需要DepP的伴侣活性而不是蛋白酶活性。高温下细胞不足。 rpoE基因的过表达，其编码负责参与细胞外应激反应的因子表达的super（E），也抑制了ssrA degP突变体的ts表型。这表明在没有SsrA的情况下，应力响应途径可能参与了degP突变体ts表型的增强。

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