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PMID: 9737855 Published · ppublish English Journal Article Research Support, U.S. Gov't, P.H.S.

Enzymological characterization of the signal-transducing uridylyltransferase/uridylyl-removing enzyme (EC 2.7.7.59) of Escherichia coli and its interaction with the PII protein.

Biochemistry ·Vol. 37 ·No. 37 ·1998-09-15 ·Pages 12782-94

Jiang P, Peliska JA, Ninfa AJ

Abstract

The uridylyltransferase/uridylyl-removing enzyme (UTase/UR) of Escherichia coli plays an important role in the regulation of nitrogen assimilation by controlling the uridylylation state of the PII signal transduction protein (PII) in response to intracellular signals. The reversible uridylylation of PII indirectly controls the activity of PII receptors that regulate transcription from nitrogen-regulated promoters and the activity of glutamine synthetase. Here, we present a detailed analysis of the uridylyltransferase and uridylyl-removing activities and their regulation by the small molecule effectors ATP, 2-ketoglutarate, and glutamine. Several important features of enzyme mechanism and regulation were elucidated. Mg2+ appeared to be the physiologically relevant metal ion cofactor for both transferase and uridylyl-removing activities. The transferase reaction proceeded by an ordered bi-bi kinetic mechanism, with PII binding before UTP and pyrophosphate (PPi) released before PII-UMP. The uridylyl-removing reaction proceeded with rapid equilibrium binding of substrate and random release of products. Both reactions were activated by ATP and 2-ketoglutarate, which did so by binding only to PII and PII-UMP. The binding of these effectors to PII and PII-UMP was characterized. Glutamine inhibited the transferase reaction by inhibiting the chemistry step, while glutamine provided nonessential mixed-type activation of the uridylyl-removing activity, lowering the apparent Km and increasing kcat. Our data were consistent with the hypothesis that all effects of glutamine are due to the binding of central complexes at a single glutamine site. By comparing the effects of the activators with their reported in vivo concentrations, we conclude that in intact cells the uridylylation state of PII is regulated mainly by the glutamine concentration and is largely independent of the 2-ketoglutarate concentration. Our kinetic data were consistent with the hypothesis that both transferase and uridylyl-removal reactions occurred at a single active center on the enzyme.

MeSH Terms
Bacterial Proteins/antagonists & inhibitors,chemistry,metabolism Binding, Competitive Cytidine Triphosphate/metabolism Enzyme Activation Escherichia coli/enzymology Glutamate-Ammonia Ligase/metabolism Glutamine/pharmacology Manganese/metabolism Nicotinamide-Nucleotide Adenylyltransferase/metabolism Nucleotidyltransferases/antagonists & inhibitors,chemistry,metabolism PII Nitrogen Regulatory Proteins Pyrimidine Nucleotides/metabolism Substrate Specificity Uridine Triphosphate/metabolism
Chemicals
Bacterial Proteins PII Nitrogen Regulatory Proteins Pyrimidine Nucleotides Glutamine Manganese PIID regulatory protein, Bacteria Cytidine Triphosphate Nucleotidyltransferases Nicotinamide-Nucleotide Adenylyltransferase regulatory protein uridylyltransferase Glutamate-Ammonia Ligase Uridine Triphosphate
Authors & Affiliations
3 authors, click to expand affiliations / ORCID
Jiang P
Department of Biological Chemistry, University of Michigan Medical School, Ann Arbor 48109-0606, USA.
Peliska J A
Ninfa A J
Article Info
Journal
Biochemistry
Abbr.
Biochemistry
ISSN
0006-2960
Published
1998-09-15
Pages
12782-94
Language
English
Region
United States
NLM ID
0370623
Subset
IM
Grants
NIGMS NIH HHS · GM47460 · United States
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