Role of the GlnK signal transduction protein in the regulation of nitrogen assimilation in Escherichia coli.
Two structurally similar but functionally distinct PII-like proteins, PII and GlnK, regulate nitrogen assimilation in Escherichia coli. Studies with cells indicated that both PII (the glnB product) and GlnK (the glnK product) acted through the kinase/phosphatase NRII [NtrB, the glnL (ntrB) product] to reduce transcription initiation from Ntr promoters, apparently by regulating the phosphorylation state of the transcriptional activator NRI-P (NtrC-P, the phosphorylated form of the glnG (ntrC) product). Both GlnK and PII also acted through adenylyltransferase (ATase, the glnE product) to regulate the adenylylation state of glutamine synthetase (GS). The activity of both GlnK and PII was regulated by the signal-transducing uridylyltransferase/uridylyl-removing enzyme (UTase/UR, glnD product). Our experiments indicate that either PII or GlnK could effectively regulate ATase, but that PII was required for the efficient regulation of NRII required to prevent expression of glnA, which encodes GS. Yet, GlnK also participated in regulation of NRII. Although cells that lack either PII or GlnK grew well, cells lacking both of these proteins were defective for growth on nitrogen-rich minimal media. This defect was alleviated by the loss of NRII, and was apparently due to unregulated expression of the Ntr regulon. Also, mutations in glnK, designated glnK*, were obtained as suppressors of the Ntr- phenotype of a double mutant lacking PII and the UTase/UR. These suppressors appeared to reduce, but not eliminate, the ability of GlnK to prevent Ntr gene expression by acting through NRII. We hypothesize that one role of GlnK is to regulate the expression of the level of NRI-P during conditions of severe nitrogen starvation, and by so doing to contribute to the regulation of certain Ntr genes.
Department of Biological Chemistry, University of Michigan Medical School, Ann Arbor 48109-0606, USA.
M R
MR
Atkinson
A J
AJ
Ninfa
D018528:ATP-Binding Cassette Transporters / Q000235:genetics / Q000378:metabolism; D000596:Amino Acids / Q000378:metabolism; D001120:Arginine / Q000378:metabolism; D001426:Bacterial Proteins / Q000235:genetics / Q000378:metabolism; D002352:Carrier Proteins / Q000235:genetics* / Q000378:metabolism*; D027682:Cation Transport Proteins; D004926:Escherichia coli / Q000235:genetics / Q000254:growth & development / Q000378:metabolism*; D029968:Escherichia coli Proteins; D015964:Gene Expression Regulation, Bacterial; D005974:Glutamate-Ammonia Ligase / Q000235:genetics / Q000378:metabolism; D009154:Mutation; D009584:Nitrogen / Q000378:metabolism*; D009713:Nucleotidyltransferases / Q000235:genetics / Q000378:metabolism; D051922:PII Nitrogen Regulatory Proteins; D010641:Phenotype; D010749:Phosphoprotein Phosphatases / Q000235:genetics / Q000378:metabolism; D011494:Protein Kinases / Q000235:genetics / Q000378:metabolism; D011993:Recombinant Fusion Proteins / Q000235:genetics / Q000378:metabolism; D015398:Signal Transduction; D001616:beta-Galactosidase / Q000235:genetics / Q000378:metabolism
D018528:ATP-Binding Cassette Transporters; D000596:Amino Acids; C111096:AmtB protein, E coli; D001426:Bacterial Proteins; D002352:Carrier Proteins; D027682:Cation Transport Proteins; D029968:Escherichia coli Proteins; C113488:GlnK protein, Azorhizobium caulinodans; D051922:PII Nitrogen Regulatory Proteins; D011993:Recombinant Fusion Proteins; C085503:mdlB protein, E coli; C404143:PIID regulatory protein, Bacteria; D001120:Arginine; D011494:Protein Kinases; C055699:protein kinase-phosphatase NTRB; D009713:Nucleotidyltransferases; C022515:regulatory protein uridylyltransferase; D010749:Phosphoprotein Phosphatases; D001616:beta-Galactosidase; C081173:glutamine synthetase I; D005974:Glutamate-Ammonia Ligase; D009584:Nitrogen