<br>fetA (ybbL) 和 fetB (ybbM) 的过表达编码铁输出蛋白，增强大肠杆菌对氧化应激的抵抗力。,Applied and Environmental Microbiology

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fetA (ybbL) 和 fetB (ybbM) 的过表达编码铁输出蛋白，增强大肠杆菌对氧化应激的抵抗力。
Applied and Environmental Microbiology ( IF 3.9 ) Pub Date : 2013-09-13 , DOI: 10.1128/aem.02322-13
Sergios A Nicolaou ₁ , Alan G Fast , Eiko Nakamaru-Ogiso , Eleftherios T Papoutsakis

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活性氧是由 H2O2 和铁的氧化还原反应和芬顿反应产生的，产生羟基自由基，导致严重的 DNA、蛋白质和脂质损伤。我们筛选了大肠杆菌基因组文库，鉴定出包含cueR、ybbJ、qmcA、ybbL 和ybbM 的片段，该片段增强了对H2O2 胁迫的抵抗力。我们报告说，ΔybbL 和 ΔybbM 菌株比亲本菌株更容易受到 H2O2 胁迫的影响，并且 ybbL 和 ybbM 过表达克服了 H2O2 敏感性。 ybbL 和 ybbM 基因预计编码 ATP 结合盒金属转运蛋白，并且我们证明 YbbM 是一种膜蛋白。我们研究了各种金属，以确定铁作为这种转运蛋白的可能底物。我们提出基因名称 fetA 和 fetB（用于铁转运）以及基因产物名称 FetA 和 FetB。 FetAB 在铁存在的情况下可以增强对氧化应激的抵抗力，揭示了铁稳态的作用。我们发现，亲本菌株和 Δfur 菌株中 fetA 和 fetB 的过表达可以消除与 H2O2 应激相关的铁超载，其中铁的摄取失调。此外，我们利用全细胞电子顺磁共振表明，通过 fetA 和 fetB 过表达，Δfur 菌株的细胞内铁水平降低了 37%。综合起来，这些研究结果表明，fetA 和 fetB 编码一种铁输出蛋白，该蛋白在增强对 H2O2 介导的氧化应激的抵抗力方面发挥作用，并且可以在铁过载条件下最大限度地减少氧化应激，并表明 FetAB 促进铁稳态以减少氧化应激。

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Overexpression of fetA (ybbL) and fetB (ybbM), Encoding an Iron Exporter, Enhances Resistance to Oxidative Stress in Escherichia coli.

Reactive oxygen species are generated by redox reactions and the Fenton reaction of H2O2 and iron that generates the hydroxyl radical that causes severe DNA, protein, and lipid damage. We screened Escherichia coli genomic libraries to identify a fragment, containing cueR, ybbJ, qmcA, ybbL, and ybbM, which enhanced resistance to H2O2 stress. We report that the ΔybbL and ΔybbM strains are more susceptible to H2O2 stress than the parent strain and that ybbL and ybbM overexpression overcomes H2O2 sensitivity. The ybbL and ybbM genes are predicted to code for an ATP-binding cassette metal transporter, and we demonstrate that YbbM is a membrane protein. We investigated various metals to identify iron as the likely substrate of this transporter. We propose the gene names fetA and fetB (for Fe transport) and the gene product names FetA and FetB. FetAB allows for increased resistance to oxidative stress in the presence of iron, revealing a role in iron homeostasis. We show that iron overload coupled with H2O2 stress is abrogated by fetA and fetB overexpression in the parent strain and in the Δfur strain, where iron uptake is deregulated. Furthermore, we utilized whole-cell electron paramagnetic resonance to show that intracellular iron levels in the Δfur strain are decreased by 37% by fetA and fetB overexpression. Combined, these findings show that fetA and fetB encode an iron exporter that has a role in enhancing resistance to H2O2-mediated oxidative stress and can minimize oxidative stress under conditions of iron overload and suggest that FetAB facilitates iron homeostasis to decrease oxidative stress.

更新日期：2019-11-01

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