RRC ID 29721
Author Pahel G, Zelenetz AD, Tyler BM.
Title gltB gene and regulation of nitrogen metabolism by glutamine synthetase in Escherichia coli.
Journal J Bacteriol
Abstract A mutant (gltB) of Escherichia coli lacking glutamate synthase (GOGAT) was unable to utilize a wide variety of compounds as sole nitrogen source (e.g., arginine, proline, gamma-aminobutyrate, and glycine). Among revertants of these Asm- strains selected on one of these compounds (e.g., arginine, proline, or gamma-aminobutyrate) were those that produce glutamine synthetase (GS) constitutively (GlnC phenotype). These revertants had a pleiotropically restored ability to grow on compounds that are metabolized to glutamate. This suggested that the expression of the genes responsible for the metabolism of these nitrogen sources was regulated by GS. An examination of the regulation of proline oxidase confirmed this hypothesis. The differential sensitivities of GlnC and wild-type strains to low concentrations (0.1 mM) of the glutamine analog L-methionine-DL-sulfoximine supported the conclusion that the synthesis of a glutamine permease was also positively controlled by GS. During the course of this study we found that the reported position of the locus (gltB) for glutamate synthase is incorrect. We have relocated this gene to be 44% linked to the argG locus by P1 transduction. Further mapping has shown that the locus previously called aspB is in reality the gltB locus and that the "suppressor" of the aspB mutation (A. M. Reiner, J. Bacteriol. 97:1431-1436, 1969) is the locus for glutamate dehydrogenase (gdhA).
Volume 133(1)
Pages 139-48
Published 1978-1-1
DOI 10.1128/JB.133.1.139-148.1978
PMID 22535
PMC PMC221987
MeSH Ammonia / metabolism Chromosome Mapping Escherichia coli / enzymology Escherichia coli / genetics* Genes* Genetic Linkage Genotype Glutamate-Ammonia Ligase / genetics* Glutamate-Ammonia Ligase / metabolism Nitrogen / metabolism* Phenotype
IF 3.234
Prokaryotes E. coli ME8701 ME8457