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首页> 外文期刊>PLoS Genetics >Global mistranslation increases cell survival under stress in Escherichia coli
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Global mistranslation increases cell survival under stress in Escherichia coli

机译：全球递药增加了在<斜体>大肠杆菌中的压力下的细胞存活率

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摘要

Mistranslation is typically deleterious for cells, although specific mistranslated proteins can confer a short-term benefit in a particular environment. However, given its large overall cost, the prevalence of high global mistranslation rates remains puzzling. Altering basal mistranslation levels of Escherichia coli in several ways, we show that generalized mistranslation enhances early survival under DNA damage, by rapidly activating the SOS response. Mistranslating cells maintain larger populations after exposure to DNA damage, and thus have a higher probability of sampling critical beneficial mutations. Both basal and artificially increased mistranslation increase the number of cells that are phenotypically tolerant and genetically resistant under DNA damage; they also enhance survival at high temperature. In contrast, decreasing the normal basal mistranslation rate reduces cell survival. This wide-ranging stress resistance relies on Lon protease, which is revealed as a key effector that induces the SOS response in addition to alleviating proteotoxic stress. The new links between error-prone protein synthesis, DNA damage, and generalised stress resistance indicate surprising coordination between intracellular stress responses and suggest a novel hypothesis to explain high global mistranslation rates.
机译：误区通常对细胞有害，尽管特定的误导性蛋白质可以在特定环境中赋予短期益处。然而，鉴于其总体成本较大，高全球误传率的普遍性仍然是令人费解的。通过多种方式改变大肠杆菌的基础误差水平，通过快速激活SOS响应，普遍的递除在DNA损伤下提高早期存活。误导细胞在暴露于DNA损伤后保持较大的群体，因此具有更高的采样临界受益突变的概率。基础和人工增加的误差均增加了在DNA损伤下表型耐受性和遗传抵抗的细胞数量;它们还在高温下增强存活。相比之下，降低正常的基础误差率降低了细胞存活率。这种宽的抗胁迫性依赖于LON蛋白酶，其揭示为诱导SOS反应的关键效应器，除了缓解蛋白毒性应激之外。易于易于蛋白质合成，DNA损伤和广义应力阻力之间的新联接表明细胞内应激反应之间的令人惊讶的协调，并提出了一种新的假设来解释高全球误差率。

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