The small protein MgtS and small RNA MgrR modulate the PitA phosphate symporter to boost intracellular magnesium levels.

In response to low levels of magnesium (Mg²⁺ ), the PhoQP two component system induces the transcription of two convergent genes, one encoding a 31-amino acid protein denoted MgtS and the second encoding a small, regulatory RNA (sRNA) denoted MgrR. Previous studies showed that the MgtS protein interacts with and stabilizes the MgtA Mg²⁺ importer to increase intracellular Mg²⁺ levels, while the MgrR sRNA base pairs with the eptB mRNA thus affecting lipopolysaccharide modification. Surprisingly, we found overexpression of the MgtS protein also leads to induction of the PhoRB regulon. Studies to understand this activation showed that MgtS forms a complex with a second protein, PitA, a cation-phosphate symporter. Given that the additive effect of ∆mgtA and ∆mgtS mutations on intracellular Mg²⁺ concentrations seen previously is lost in the ∆pitA mutant, we suggest that MgtS binds to and prevents Mg²⁺ leakage through PitA under Mg²⁺ -limiting conditions. Consistent with a detrimental role of PitA in low Mg²⁺ , we also observe MgrR sRNA repression of PitA synthesis. Thus, PhoQP induces the expression of two convergent small genes in response to Mg²⁺ limitation whose products act to modulate PitA at different levels to increase intracellular Mg²⁺ .

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