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首页> 外文期刊>Journal of Molecular Biology >Toxin-antitoxin loci as stress-response-elements: ChpAK/MazF and ChpBK cleave translated RNAs and are counteracted by tmRNA.
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Toxin-antitoxin loci as stress-response-elements: ChpAK/MazF and ChpBK cleave translated RNAs and are counteracted by tmRNA.

机译：毒素-抗毒素基因座作为应激反应元件：ChpAK / MazF和ChpBK裂解翻译的RNA，并被tmRNA抵消。

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摘要

Prokaryotic chromosomes encode toxin-antitoxin loci, often in multiple copies. In most cases, the function of these genes is not known. The chpA (mazEF) locus of Escherichia coli has been described as a cell killing module that induces bacterial apoptosis during nutritional stress. However, we found recently that ChpAK (MazF) does not confer cell killing but rather, induces a bacteriostatic condition from which the cells could be resuscitated. Results presented here yield a mechanistic explanation for the detrimental effect on cell growth exerted by ChpAK and the homologous ChpBK protein of E.coli. We show that both proteins inhibit translation by inducing cleavage of translated mRNAs. Consistently, the inhibitory effect of the proteins was counteracted by tmRNA. Amino acid starvation induced strong transcription of chpA that depended on Lon protease but not on ppGpp. Simultaneously, ChpAK cleaved tmRNA in its coding region. Thus, ChpAK and ChpBK inhibit translation by a mechanism very similar to that of E.coli RelE. On the basis of these results, we propose a model that integrates TA loci into general prokaryotic stress physiology.
机译：原核染色体编码毒素-抗毒素基因座，通常是多个拷贝。在大多数情况下，这些基因的功能尚不清楚。大肠杆菌的chpA（mazEF）位点已被描述为一种细胞杀伤模块，可在营养胁迫期间诱导细菌凋亡。但是，我们最近发现ChpAK（MazF）不会导致细胞杀伤，而是会诱导抑菌条件，从中可以恢复细胞。此处给出的结果为ChpAK和大肠杆菌的同源ChpBK蛋白对细胞生长的有害作用提供了机械解释。我们表明这两种蛋白通过诱导翻译的mRNA的切割抑制翻译。一致地，tmRNA抵消了蛋白质的抑制作用。氨基酸饥饿诱导了chpA的强转录，该转录依赖于Lon蛋白酶而不依赖于ppGpp。同时，ChpAK在其编码区切割了tmRNA。因此，ChpAK和ChpBK通过与大肠杆菌RelE非常相似的机制抑制翻译。在这些结果的基础上，我们提出了一个将TA基因座整合到一般原核应激生理中的模型。

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