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rdf:type |
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lifeskim:mentions |
umls-concept:C0004595,
umls-concept:C0038952,
umls-concept:C0178539,
umls-concept:C0205463,
umls-concept:C0241938,
umls-concept:C0439799,
umls-concept:C0805586,
umls-concept:C0871261,
umls-concept:C1704632,
umls-concept:C1706817,
umls-concept:C1880177,
umls-concept:C2911692
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pubmed:issue |
8
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pubmed:dateCreated |
2008-4-10
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pubmed:abstractText |
Mechanosensitive channels are thought to function as safety valves for the release of cytoplasmic solutes from cells that have to manage a rapid transition from high- to low-osmolarity environments. Subsequent to an osmotic down-shock of cells grown at high osmolarity, Bacillus subtilis rapidly releases the previously accumulated compatible solute glycine betaine in accordance with the degree of the osmotic downshift. Database searches suggest that B. subtilis possesses one copy of a gene for a mechanosensitive channel of large conductance (mscL) and three copies of genes encoding proteins that putatively form mechanosensitive channels of small conductance (yhdY, yfkC, and ykuT). Detailed mutational analysis of all potential channel-forming genes revealed that a quadruple mutant (mscL yhdY yfkC ykuT) has no growth disadvantage in high-osmolarity media in comparison to the wild type. Osmotic down-shock experiments demonstrated that the MscL channel is the principal solute release system of B. subtilis, and strains with a gene disruption in mscL exhibited a severe survival defect upon an osmotic down-shock. We also detected a minor contribution of the SigB-controlled putative MscS-type channel-forming protein YkuT to cellular survival in an mscL mutant. Taken together, our data revealed that mechanosensitive channels of both the MscL and MscS types play pivotal roles in managing the transition of B. subtilis from hyper- to hypo-osmotic environments.
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pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/18310427-10066837,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18310427-10202137,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18310427-10216873,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18310427-10322175,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18310427-10498951,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18310427-11275684,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18310427-11544224,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18310427-11902719,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18310427-12446901,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18310427-12626684,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18310427-12767977,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18310427-1350764,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18310427-1383039,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18310427-1384708,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18310427-14015559,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18310427-15613476,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18310427-16493417,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18310427-16897034,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18310427-1692209,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18310427-17505523,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18310427-7511799,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18310427-7622480,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18310427-7988888,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18310427-8297208,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18310427-8752321,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18310427-8973347,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18310427-9266699,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18310427-9632260,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18310427-9670799,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18310427-9818351,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18310427-9856938
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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 |
Apr
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pubmed:issn |
1098-5336
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pubmed:author |
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pubmed:issnType |
Electronic
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pubmed:volume |
74
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
2454-60
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pubmed:dateRevised |
2009-11-18
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pubmed:meshHeading |
pubmed-meshheading:18310427-Bacillus subtilis,
pubmed-meshheading:18310427-Bacterial Proteins,
pubmed-meshheading:18310427-Betaine,
pubmed-meshheading:18310427-Gene Deletion,
pubmed-meshheading:18310427-Gene Order,
pubmed-meshheading:18310427-Ion Channels,
pubmed-meshheading:18310427-Mechanotransduction, Cellular,
pubmed-meshheading:18310427-Microbial Viability,
pubmed-meshheading:18310427-Mutagenesis, Insertional,
pubmed-meshheading:18310427-Osmotic Pressure
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pubmed:year |
2008
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pubmed:articleTitle |
Responses of Bacillus subtilis to hypotonic challenges: physiological contributions of mechanosensitive channels to cellular survival.
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pubmed:affiliation |
Philipps University Marburg, Department of Biology, Laboratory for Microbiology, Karl-von-Frisch-Str., D-35032 Marburg, Federal Republic of Germany.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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