期刊
MOLECULAR MICROBIOLOGY
卷 111, 期 1, 页码 131-144出版社
WILEY
DOI: 10.1111/mmi.14143
关键词
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资金
- Intramural Research Program of the Eunice Kennedy Shriver National Institute of Child Health and Human Development
- Pharmacology Research Associate Program of the National Institute of General Medical Sciences
- Intramural Research Program of the National Library of Medicine
- EUNICE KENNEDY SHRIVER NATIONAL INSTITUTE OF CHILD HEALTH & HUMAN DEVELOPMENT [ZIAHD001608, ZIAHD008855] Funding Source: NIH RePORTER
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 increment mgtA and increment mgtS mutations on intracellular Mg2+ concentrations seen previously is lost in the increment 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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