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Nickel exposure reduces enterobactin production in Escherichia coli

机译:镍暴露在大肠杆菌中减少肠酰胺生产

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摘要

Escherichia coli is a well‐studied bacterium that can be found in many niches, such as industrial wastewater, where the concentration of nickel can rise to low‐millimolar levels. Recent studies show that nickel exposure can repress pyochelin or induce pyoverdine siderophore production in Pseudomonas aueroginosa . Understanding the molecular cross‐talk between siderophore production, metal homeostasis, and metal toxicity in microorganisms is critical for designing bioremediation strategies for metal‐contaminated sites. Here, we show that high‐nickel exposure prolongs lag phase duration as a result of low‐intracellular iron levels in E.?coli . Although E.?coli cells respond to low‐intracellular iron during nickel stress by maintaining high expression of iron uptake systems such as fepA , the demand for iron is not met due to a lack of siderophores in the extracellular medium during nickel stress. Taken together, these results indicate that nickel inhibits iron accumulation in E.?coli by reducing the presence of enterobactin in the extracellular medium.
机译:大肠杆菌是一种学习的细菌,可以在许多核酸中找到,例如工业废水,其中镍浓度可以升高到低毫摩尔水平。最近的研究表明,镍暴露可以抑制肥胖的血液素或诱导肥胖的岩石植物生成葡萄球菌。了解微生物中的金属稳态和金属毒性之间的分子串扰,对于设计金属污染部位的生物修复策略至关重要。在这里,我们表明,由于E.?Coli的低细胞内铁水平,高镍暴露延长滞后阶段持续时间。虽然E.?COLI细胞通过维持诸如FEPA的铁摄取系统的高表达,但是在镍应力期间响应低细胞内铁,但由于在镍应力期间缺乏细胞外介质中的散发体,对铁的需求不会满足。总之,这些结果表明镍通过减少细胞外培养基中的肠酰胺的存在来抑制E.?Coli中的铁积累。

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