Nickel exposure reduces enterobactin production in Escherichia coli

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. Toxic nickel exposure reduces iron accumulation in lag phase Escherichia coli Nickel appears directly or indirectly to target siderophore metabolism in E. coli, thereby reducing levels of enterobactin and its hydrolysis products in the extracellular environment.