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rdf:type |
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lifeskim:mentions |
umls-concept:C0007367,
umls-concept:C0010798,
umls-concept:C0011155,
umls-concept:C0014834,
umls-concept:C0018270,
umls-concept:C0031437,
umls-concept:C0038952,
umls-concept:C0080194,
umls-concept:C0205202,
umls-concept:C0205228,
umls-concept:C0376446,
umls-concept:C0678226
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pubmed:issue |
21
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pubmed:dateCreated |
1997-1-13
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pubmed:abstractText |
The cydDC operon of Escherichia coli encodes an ATP-dependent transporter of unknown function that is required for cytochrome bd synthesis. Strains containing defects in either the cydD or cydC gene also demonstrate hypersensitivity to growth at high temperatures and the inability to exit the stationary phase at 37 degrees C. We wished to determine what is responsible for these hypersensitive phenotypes and whether they are due to a lack of the CydDC proteins or a defect of the cytochrome bd encoded by the cydAB genes. Using both K-12- and B-type strains of E. coli, we have compared the phenotypes of isogenic cydAB mutants and cydC mutants. In both K-12- and B-type backgrounds, the hypersensitive phenotypes are due to defects of cytochrome bd activity and not defects of the cydDC genes. We also found that the temperature-sensitive growth phenotypes can be suppressed by exogenous reducing agents, such as glutathione and cysteine. Strikingly, even the enzymes catalase and superoxide dismutase, when added exogenously, can correct the temperature-sensitive and stationary phase arrest phenotypes. We propose that the temperature sensitive growth phenotypes are due to a buildup of diffusible oxygen radicals brought on by the absence of cytochrome bd.
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pubmed:grant |
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pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/8892839-1310500,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8892839-1328158,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8892839-1355616,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8892839-1655701,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8892839-2170337,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8892839-2559153,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8892839-3032907,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8892839-3036876,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8892839-7934832,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8892839-8181727,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8892839-8276245,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8892839-8380150,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8892839-8626323,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8892839-8830242,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8892839-8892838
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
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pubmed:status |
MEDLINE
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pubmed:month |
Nov
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pubmed:issn |
0021-9193
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:volume |
178
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
6348-51
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pubmed:dateRevised |
2009-11-18
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pubmed:meshHeading |
pubmed-meshheading:8892839-ATP-Binding Cassette Transporters,
pubmed-meshheading:8892839-Catalase,
pubmed-meshheading:8892839-Cytochromes,
pubmed-meshheading:8892839-Electron Transport Chain Complex Proteins,
pubmed-meshheading:8892839-Escherichia coli,
pubmed-meshheading:8892839-Escherichia coli Proteins,
pubmed-meshheading:8892839-Gene Expression Regulation, Bacterial,
pubmed-meshheading:8892839-Oxidoreductases,
pubmed-meshheading:8892839-Phenotype,
pubmed-meshheading:8892839-Reducing Agents,
pubmed-meshheading:8892839-Superoxide Dismutase,
pubmed-meshheading:8892839-Temperature
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pubmed:year |
1996
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pubmed:articleTitle |
The temperature-sensitive growth and survival phenotypes of Escherichia coli cydDC and cydAB strains are due to deficiencies in cytochrome bd and are corrected by exogenous catalase and reducing agents.
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pubmed:affiliation |
Department of Biology, Washington University, St. Louis, MO 63130, USA.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.
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