首页> 外文期刊>Molecular Microbiology >Protection of the DNA during the exposure of Escherichia coli cells to a toxic metabolite: the role of the KefB and KefC potassium channels.
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Protection of the DNA during the exposure of Escherichia coli cells to a toxic metabolite: the role of the KefB and KefC potassium channels.

机译:在大肠杆菌细胞暴露于有毒代谢产物期间对DNA的保护:KefB和KefC钾通道的作用。

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摘要

The effect of the toxic metabolite methylglyoxal on the DNA of Escherichia coli cells has been investigated. Exposure of E. coli cells to methylglyoxal reduces the transformability of plasmid DNA and results in the degradation of genomic DNA. The activity of the KefB and KefC potassium channels protects E. coli cells against methylglyoxal and limits the amount of DNA damage. In mutants lacking KefB and KefC, methylglyoxal-induced DNA damage was reduced by incubation with a weak acid that lowers the pHi to the same extent as through KefB and KefC activation. This provides evidence that acidification of the cytoplasm protects E. coli DNA against methylglyoxal. By the analysis of cells lacking UvrA, we demonstrate that this repair protein is required for the degradation of the DNA upon methylglyoxal exposure. However, protection by KefB and KefC occurred independently of UvrA. Although we present evidence that exposure of E. coli cells to methylglyoxal results in DNA degradation, our results suggest this event is not essential for methylglyoxal-induced death. The implications of these findings will be discussed.
机译:已经研究了有毒代谢产物甲基乙二醛对大肠杆菌细胞DNA的影响。大肠杆菌细胞暴露于甲基乙二醛会降低质粒DNA的转化能力,并导致基因组DNA降解。 KefB和KefC钾通道的活性可保护大肠杆菌细胞免受甲基乙二醛的侵害并限制DNA损伤的程度。在缺乏KefB和KefC的突变体中,通过与弱酸孵育降低了甲基乙二醛诱导的DNA损伤,弱酸将pHi降低到与通过KefB和KefC激活相同的程度。这提供了证据,表明细胞质的酸化可以保护大肠杆菌DNA免受甲基乙二醛的侵害。通过分析缺乏UvrA的细胞,我们证明了这种修复蛋白是甲基乙二醛暴露后降解DNA所必需的。但是,KefB和KefC的保护独立于UvrA发生。尽管我们提供证据表明大肠杆菌细胞暴露于甲基乙二醛会导致DNA降解,但我们的结果表明该事件对于甲基乙二醛诱导的死亡并非必需。这些发现的含义将进行讨论。

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