PMID:353047: Difference between revisions

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<span style = 'font-size: large'> '''Pluschke, G, Hirota, Y and Overath, P'''  (1978) Function of phospholipids in Escherichia coli. Characterization of a mutant deficient in cardiolipin synthesis.''J. Biol. Chem.'' '''253''':5048-55</span>
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!align=left  |Citation
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'''No author listed'''  (1978) Function of phospholipids in Escherichia coli. Characterization of a mutant deficient in cardiolipin synthesis. ''J. Biol. Chem.'' '''253''':5048-55
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!align=left  |Abstract
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Screening of a collection of temperature-sensitive mutants of Escherichia coli for defects in phospholipid metabolism led to the isolation of a mutant deficient in cardiolipin synthesis. The defective gene, named cls, is closely linked to the trp marker and maps at about Minute 27 on the E. coli chromosome. After transfer of cls to a defined genetic background by transduction, the mutant has the following properties as compared to an isogenic wild type. Exponentially growing cells show a reduction in cardiolipin content by a factor of at least 15 (less than 0.2 mol % of the total phospholipids). A crude membrane fraction derived from the mutant is unable to synthesize cardiolipin from phosphatidylglycerol in vitro. The mutant has no distinctive phenotype regarding its growth properties, membrane-associated respiratory functions, or the ability to insert bacteriophage M13 coat protein into the cell envelope. The cls mutation confers a 5-times reduction in the turnover of the phosphate moiety of phosphatidylglycerol.
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[http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=353047 PubMed]


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|{{TableHeadingColor}} |'''Abstract''' || <protect>Screening of a collection of temperature-sensitive mutants of Escherichia coli for defects in phospholipid metabolism led to the isolation of a mutant deficient in cardiolipin synthesis. The defective gene, named cls, is closely linked to the trp marker and maps at about Minute 27 on the E. coli chromosome. After transfer of cls to a defined genetic background by transduction, the mutant has the following properties as compared to an isogenic wild type. Exponentially growing cells show a reduction in cardiolipin content by a factor of at least 15 (less than 0.2 mol % of the total phospholipids). A crude membrane fraction derived from the mutant is unable to synthesize cardiolipin from phosphatidylglycerol in vitro. The mutant has no distinctive phenotype regarding its growth properties, membrane-associated respiratory functions, or the ability to insert bacteriophage M13 coat protein into the cell envelope. The cls mutation confers a 5-times reduction in the turnover of the phosphate moiety of phosphatidylglycerol.</protect>
!align=left  |Keywords
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|{{TableHeadingColor}} nowrap |'''Links''' ||  [http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=353047 PubMed]<br/>
Cardiolipins/biosynthesis; Chromosome Mapping; Coliphages/metabolism; Escherichia coli/metabolism; Genes; Mutation; Phospholipids/metabolism; Species Specificity; Transduction, Genetic
 
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==Significance {{HelpIcon|Help:Literature}} ==
==Significance {{HelpIcon|Help:Literature}} ==
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Revision as of 19:25, 1 September 2013

Citation

No author listed (1978) Function of phospholipids in Escherichia coli. Characterization of a mutant deficient in cardiolipin synthesis. J. Biol. Chem. 253:5048-55

Abstract

Screening of a collection of temperature-sensitive mutants of Escherichia coli for defects in phospholipid metabolism led to the isolation of a mutant deficient in cardiolipin synthesis. The defective gene, named cls, is closely linked to the trp marker and maps at about Minute 27 on the E. coli chromosome. After transfer of cls to a defined genetic background by transduction, the mutant has the following properties as compared to an isogenic wild type. Exponentially growing cells show a reduction in cardiolipin content by a factor of at least 15 (less than 0.2 mol % of the total phospholipids). A crude membrane fraction derived from the mutant is unable to synthesize cardiolipin from phosphatidylglycerol in vitro. The mutant has no distinctive phenotype regarding its growth properties, membrane-associated respiratory functions, or the ability to insert bacteriophage M13 coat protein into the cell envelope. The cls mutation confers a 5-times reduction in the turnover of the phosphate moiety of phosphatidylglycerol.

Links

PubMed

Keywords

Cardiolipins/biosynthesis; Chromosome Mapping; Coliphages/metabolism; Escherichia coli/metabolism; Genes; Mutation; Phospholipids/metabolism; Species Specificity; Transduction, Genetic

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Significance

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Useful Materials and Methods

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Annotations

Gene product Qualifier GO ID GO term name Evidence Code with/from Aspect Notes Status

Cls

GO:0008808

cardiolipin synthase activity

IMP: Inferred from Mutant Phenotype

F

complete

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