Difference between revisions of "PMID:4905670"

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{|  id="D4d067c6d1367f"  class=" tableEdit PMID_info_table" 
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!align=left  |Citation
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'''Wong, PT, Kashket, ER and Wilson, TH'''  (1970) Energy coupling in the lactose transport system of Escherichia coli.''Proc. Natl. Acad. Sci. U.S.A.'' '''65''':63-9
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!align=left  |Abstract
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A mutant (ML 308-22) was isolated from Escherichia coli ML 308, which had lost the normal capacity to accumulate lactose analogs despite an increase in the membrane carrier activity. The exit of thiomethylgalactoside was much faster than normal, accounting for the inability of the cell to maintain high intracellular concentrations of galactosides. Growth of the mutant on lactose was normal at high concentrations of sugar and impaired at low concentrations. This transport defect appeared to be limited to the lactose transport system as D-fucose and alpha-aminoisobutyric acid uptake and accumulation were normal. It is inferred from the data that the mutant possessed a defect in the coupling of metabolic energy to lactose transport.
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[http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=4905670 PubMed]
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!align=left  |Keywords
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Aminoisobutyric Acids; Biological Transport, Active; Carbon Isotopes; Escherichia coli; Fucose; Genetics, Microbial; Glycosides; Lactose; Mutation
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==Main Points of the Paper ==
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{{LitSignificance}}
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== Materials and Methods Used ==
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{{LitMaterials}}
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==Phenotype Annotations==
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{|  id="U4d067c6d14b4c"  class=" tableEdit PMID_Phenotype_table" 
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!|Species!!Taxon ID!!Strain!!Gene (if known)!!OMP!!Phenotype!!Details!!Evidence!!Notes
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==Notes==
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<references/>

Revision as of 15:05, 13 December 2010

Citation

Wong, PT, Kashket, ER and Wilson, TH (1970) Energy coupling in the lactose transport system of Escherichia coli.Proc. Natl. Acad. Sci. U.S.A. 65:63-9

Abstract

A mutant (ML 308-22) was isolated from Escherichia coli ML 308, which had lost the normal capacity to accumulate lactose analogs despite an increase in the membrane carrier activity. The exit of thiomethylgalactoside was much faster than normal, accounting for the inability of the cell to maintain high intracellular concentrations of galactosides. Growth of the mutant on lactose was normal at high concentrations of sugar and impaired at low concentrations. This transport defect appeared to be limited to the lactose transport system as D-fucose and alpha-aminoisobutyric acid uptake and accumulation were normal. It is inferred from the data that the mutant possessed a defect in the coupling of metabolic energy to lactose transport.

Links

PubMed

Keywords

Aminoisobutyric Acids; Biological Transport, Active; Carbon Isotopes; Escherichia coli; Fucose; Genetics, Microbial; Glycosides; Lactose; Mutation

Main Points of the Paper

Please summarize the main points of the paper.

Materials and Methods Used

Please list the materials and methods used in this paper (strains, plasmids, antibodies, etc).

Phenotype Annotations

<protect>

Species Taxon ID Strain Gene (if known) OMP Phenotype Details Evidence Notes

</protect>

Notes