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Messing up translation from the start: How AtaT inhibits translation initiation in E.coli

机译:从一开始就弄乱翻译:Atat如何抑制在大肠杆菌中的翻译开始

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摘要

Toxin-antitoxin systems (TA) are widespread in bacteria and archea. They are commonly found in chromosomes and mobile genetic elements. These systems move from different genomic locations and bacterial hosts through horizontal gene transfer, using mobile elements as vehicles. Their potential roles in bacterial physiology are still a matter of debate in the field. The mechanisms of action of different toxin families have been deciphered at the molecular level. Intriguingly, the vast majority of these toxins target protein synthesis. They use a variety of molecular mechanisms and inhibit nearly every step of the translation process. Recently, we have identified a novel toxin, AtaT, presenting acetyltransferase activity. 1 Our work uncovered the molecular activity of AtaT: it specifically acetylates the methionine moiety on the initiator Met-tRNAfMet. This modification drastically impairs recognition by initiation factor 2 (IF2), thereby inhibiting the initiation step of translation.
机译:毒素 - 抗毒素系统(TA)在细菌和archea中是普遍的。 它们通常在染色体和移动遗传元素中发现。 这些系统通过水平基因转移从不同的基因组位置和细菌宿主移动,使用移动元件作为车辆。 细菌生理中的潜在作用仍然是该领域辩论的问题。 不同毒素家族的作用机制已在分子水平中破译。 有趣的是,绝大多数这些毒素靶蛋白合成。 他们使用各种分子机制并抑制翻译过程的几乎每一步。 最近,我们鉴定了一种新型毒素,Atat,呈递乙酰转移酶活性。 1我们的工作发现了Atat的分子活性:它特别是甲硫氨酸部分在引发剂Met-Trnafmet上。 该修改通过发起因子2(IF2)大大损害识别,从而抑制翻译的启动步骤。

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