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The global transcriptional response of Bacillus subtilis to manganese involves the MntR, Fur, TnrA and σ B regulons
Author(s) -
Guedon Emmanuel,
Moore Charles M.,
Que Qiang,
Wang Tao,
Ye Rick W.,
Helmann John D.
Publication year - 2003
Publication title -
molecular microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.857
H-Index - 247
eISSN - 1365-2958
pISSN - 0950-382X
DOI - 10.1046/j.1365-2958.2003.03648.x
Subject(s) - regulon , psychological repression , biology , bacillus subtilis , glutamine synthetase , repressor , biochemistry , enzyme , operon , phosphatase , glutamine , derepression , microbiology and biotechnology , regulation of gene expression , gene expression , gene , genetics , amino acid , bacteria , escherichia coli
Summary We have used DNA microarrays to monitor the global transcriptional response of Bacillus subtilis to changes in manganese availability. Mn(II) leads to the MntR‐dependent repression of both the mntH and mntABCD operons encoding Mn(II) uptake systems. Mn(II) also represses the Fur regulon. This repression is unlikely to be a direct effect of Mn(II) on Fur as repression is sensitive to 2,2′‐dipyridyl, an iron‐selective chelator. We suggest that elevated Mn(II) displaces iron from cellular‐binding sites and the resulting rise in free iron levels leads to repression of the Fur regulon. Many of the genes induced by Mn(II) are activated by σ B or TnrA. Both of these regulators are controlled by Mn(II)‐dependent enzymes. Induction of the σ B ‐dependent general stress response by Mn(II) is largely dependent on RsbU, a Mn(II)‐dependent phosphatase that dephosphorylates RsbV, ultimately leading to release of active σ B from its antisigma, RsbW. The activity of TnrA is inhibited when it forms an inactive complex with feedback‐inhibited glutamine synthetase. Elevated Mn(II) reduces the sensitivity of glutamine synthetase to feedback inhibitors, and we suggest that this leads to the observed increase in TnrA activity. In sum, three distinct mechanisms can account for most of the transcriptional effects elicited by manganese: (i) direct binding of Mn(II) to metalloregulators such as MntR, (ii) perturbation of cellular iron pools leading to increased Fur activity and (iii) altered activity of Mn(II)‐dependent enzymes that regulate the activity of σ B and TnrA.