Loss of CorA, the primary magnesium transporter of Salmonella, is alleviated by MgtA and PhoP-dependent compensatory mechanisms
Résumé
In many Gram-negative bacteria, the stress sigma factor of RNA polymerase, σ S /RpoS, remodels global gene expression to reshape the physiology of stationary phase cells and ensure their survival under non-optimal growth conditions. In the foodborne pathogen Salmonella enterica serovar Typhimurium, σ S is also required for biofilm formation and virulence. We have recently shown that a Δ rpoS mutation decreases the magnesium content and expression level of the housekeeping Mg 2+ -transporter CorA in stationary phase Salmonella . The other two Mg 2+ -transporters of Salmonella are encoded by the PhoP-activated mgtA and mgtB genes and are expressed under magnesium starvation. The σ S control of corA prompted us to evaluate the impact of CorA in stationary phase Salmonella cells, by using global and analytical proteomic analyses and physiological assays. The Δ corA mutation conferred a competitive disadvantage to exit from stationary phase, and slightly impaired motility, but had no effect on total and free cellular magnesium contents. In contrast to the wild-type strain, the Δ corA mutant produced MgtA, but not MgtB, in the presence of high extracellular magnesium concentration. Under these conditions, MgtA production in the Δ corA mutant did not require PhoP. Consistently, a Δ mgtA , but not a Δ phoP , mutation slightly reduced the magnesium content of the Δ corA mutant. Synthetic phenotypes were observed when the Δ phoP and Δ corA mutations were combined, including a strong reduction in growth and motility, independently of the extracellular magnesium concentration. The abundance of several proteins involved in flagella formation, chemotaxis and secretion was lowered by the Δ corA and Δ phoP mutations in combination, but not alone. These findings unravel the importance of PhoP-dependent functions in the absence of CorA when magnesium is sufficient. Altogether, our data pinpoint a regulatory network, where the absence of CorA is sensed by the cell and compensated by MgtA and PhoP- dependent mechanisms.
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