PMID:2017136: Difference between revisions

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<span style = 'font-size: large'> '''Kalman, M, Gentry, DR and Cashel, M'''  (1991) Characterization of the Escherichia coli K12 gltS glutamate permease gene.''Mol. Gen. Genet.'' '''225''':379-86</span>
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!align=left  |Citation
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'''Kalman, M, Gentry, DR and Cashel, M'''  (1991) Characterization of the Escherichia coli K12 gltS glutamate permease gene. ''Mol. Gen. Genet.'' '''225''':379-86
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!align=left  |Abstract
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The gltS gene is known to encode a sodium-dependent, glutamate-specific permease. We have localized the Escherichia coli K12 gltS gene with respect to the spoT gene, sequenced it, and recombined a null insertion-deletion allele into the chromosome without loss of viability. The gltS null allele gives a Glt- phenotype, i.e. it abolishes the ability of a gltCc host to grow on glutamate as sole carbon and nitrogen source and also confers alpha-methylglutamate resistance. A multicopy plasmid expressing the gltS gene can reverse the Glt- phenotype of gltS- or wild-type strains while other plasmids show host-dependent complementation patterns. Induction of gltS gene overexpression under control of isopropyl-beta-D-thiogalactoside (IPTG)-inducible promoters severely inhibits growth. The GltS protein is deduced to be a 42425 dalton hydrophobic protein with 2 sets of 5 possible integral protein domains, each flanking a central hydrophilic, flexible region.
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[http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=2017136 PubMed]


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|{{TableHeadingColor}} |'''Abstract''' || The gltS gene is known to encode a sodium-dependent, glutamate-specific permease. We have localized the Escherichia coli K12 gltS gene with respect to the spoT gene, sequenced it, and recombined a null insertion-deletion allele into the chromosome without loss of viability. The gltS null allele gives a Glt- phenotype, i.e. it abolishes the ability of a gltCc host to grow on glutamate as sole carbon and nitrogen source and also confers alpha-methylglutamate resistance. A multicopy plasmid expressing the gltS gene can reverse the Glt- phenotype of gltS- or wild-type strains while other plasmids show host-dependent complementation patterns. Induction of gltS gene overexpression under control of isopropyl-beta-D-thiogalactoside (IPTG)-inducible promoters severely inhibits growth. The GltS protein is deduced to be a 42425 dalton hydrophobic protein with 2 sets of 5 possible integral protein domains, each flanking a central hydrophilic, flexible region.
!align=left  |Keywords
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Alleles; Amino Acid Sequence; Amino Acid Transport Systems, Acidic; Base Sequence; DNA, Bacterial; Escherichia coli/drug effects; Escherichia coli/enzymology; Escherichia coli/genetics; Escherichia coli/growth & development; Escherichia coli Proteins; Frameshift Mutation; Genes, Bacterial; Genetic Complementation Test; Genetic Linkage; Glutamates/metabolism; Glutamates/pharmacology; Isopropyl Thiogalactoside/genetics; Membrane Transport Proteins/genetics; Membrane Transport Proteins/metabolism; Molecular Sequence Data; Open Reading Frames; Phenotype; Plasmids; Polymerase Chain Reaction; Promoter Regions, Genetic; Restriction Mapping; Symporters
|{{TableHeadingColor}} nowrap |'''Links''' ||  [http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=2017136 PubMed]
 
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Latest revision as of 04:36, 15 September 2013

Citation

Kalman, M, Gentry, DR and Cashel, M (1991) Characterization of the Escherichia coli K12 gltS glutamate permease gene. Mol. Gen. Genet. 225:379-86

Abstract

The gltS gene is known to encode a sodium-dependent, glutamate-specific permease. We have localized the Escherichia coli K12 gltS gene with respect to the spoT gene, sequenced it, and recombined a null insertion-deletion allele into the chromosome without loss of viability. The gltS null allele gives a Glt- phenotype, i.e. it abolishes the ability of a gltCc host to grow on glutamate as sole carbon and nitrogen source and also confers alpha-methylglutamate resistance. A multicopy plasmid expressing the gltS gene can reverse the Glt- phenotype of gltS- or wild-type strains while other plasmids show host-dependent complementation patterns. Induction of gltS gene overexpression under control of isopropyl-beta-D-thiogalactoside (IPTG)-inducible promoters severely inhibits growth. The GltS protein is deduced to be a 42425 dalton hydrophobic protein with 2 sets of 5 possible integral protein domains, each flanking a central hydrophilic, flexible region.

Links

PubMed

Keywords

Alleles; Amino Acid Sequence; Amino Acid Transport Systems, Acidic; Base Sequence; DNA, Bacterial; Escherichia coli/drug effects; Escherichia coli/enzymology; Escherichia coli/genetics; Escherichia coli/growth & development; Escherichia coli Proteins; Frameshift Mutation; Genes, Bacterial; Genetic Complementation Test; Genetic Linkage; Glutamates/metabolism; Glutamates/pharmacology; Isopropyl Thiogalactoside/genetics; Membrane Transport Proteins/genetics; Membrane Transport Proteins/metabolism; Molecular Sequence Data; Open Reading Frames; Phenotype; Plasmids; Polymerase Chain Reaction; Promoter Regions, Genetic; Restriction Mapping; Symporters

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