pubmed-article:11679074 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:11679074 | lifeskim:mentions | umls-concept:C0038411 | lld:lifeskim |
pubmed-article:11679074 | lifeskim:mentions | umls-concept:C0026882 | lld:lifeskim |
pubmed-article:11679074 | lifeskim:mentions | umls-concept:C1136170 | lld:lifeskim |
pubmed-article:11679074 | lifeskim:mentions | umls-concept:C0001721 | lld:lifeskim |
pubmed-article:11679074 | lifeskim:mentions | umls-concept:C0018270 | lld:lifeskim |
pubmed-article:11679074 | lifeskim:mentions | umls-concept:C0017262 | lld:lifeskim |
pubmed-article:11679074 | lifeskim:mentions | umls-concept:C0560137 | lld:lifeskim |
pubmed-article:11679074 | lifeskim:mentions | umls-concept:C2911684 | lld:lifeskim |
pubmed-article:11679074 | lifeskim:mentions | umls-concept:C0185117 | lld:lifeskim |
pubmed-article:11679074 | pubmed:issue | 1 | lld:pubmed |
pubmed-article:11679074 | pubmed:dateCreated | 2001-10-26 | lld:pubmed |
pubmed-article:11679074 | pubmed:abstractText | Adaptive responses of bacteria that involve sensing the presence of other bacteria are often critical for proliferation and the expression of virulence characteristics. The autoinducer II (AI-2) pathway has recently been shown to be a mechanism for sensing other bacteria that is highly conserved among diverse bacterial species, including Gram-positive pathogens. However, a role for this pathway in the regulation of virulence factors in Gram-positive pathogens has yet to be established. In this study, we have inactivated luxS, an essential component of the AI-2 pathway, in the Gram-positive pathogen Streptococcus pyogenes. Analyses of the resulting mutants revealed the aberrant expression of several virulence properties that are regulated in response to growth phase, including enhanced haemolytic activity, and a dramatic reduction in the expression of secreted proteolytic activity. This latter defect was associated with a reduced ability to secrete and process the precursor of the cysteine protease (SpeB) as well as a difference in the timing of expression of the protease. Enhanced haemolytic activity of the luxS strain was also shown to be linked with an increased expression of the haemolysin S-associated gene sagA. Disruptions of luxS in these mutants also produced a media-dependent growth defect. Finally, an allelic replacement analysis of an S. pyogenes strain with a naturally occurring insertion of IS1239 in luxS suggested a mechanism for modulation of virulence during infection. Results from this study suggest that luxS makes an important contribution to the regulation of S. pyogenes virulence factors. | lld:pubmed |
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pubmed-article:11679074 | pubmed:language | eng | lld:pubmed |
pubmed-article:11679074 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11679074 | pubmed:citationSubset | IM | lld:pubmed |
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pubmed-article:11679074 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:11679074 | pubmed:month | Oct | lld:pubmed |
pubmed-article:11679074 | pubmed:issn | 0950-382X | lld:pubmed |
pubmed-article:11679074 | pubmed:author | pubmed-author:SteimJ MJM | lld:pubmed |
pubmed-article:11679074 | pubmed:author | pubmed-author:CaparonM GMG | lld:pubmed |
pubmed-article:11679074 | pubmed:author | pubmed-author:LevinJ CJC | lld:pubmed |
pubmed-article:11679074 | pubmed:author | pubmed-author:LyonW RWR | lld:pubmed |
pubmed-article:11679074 | pubmed:author | pubmed-author:MaddenJ CJC | lld:pubmed |
pubmed-article:11679074 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:11679074 | pubmed:volume | 42 | lld:pubmed |
pubmed-article:11679074 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:11679074 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:11679074 | pubmed:pagination | 145-57 | lld:pubmed |
pubmed-article:11679074 | pubmed:dateRevised | 2007-11-14 | lld:pubmed |
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pubmed-article:11679074 | pubmed:meshHeading | pubmed-meshheading:11679074... | lld:pubmed |
pubmed-article:11679074 | pubmed:year | 2001 | lld:pubmed |
pubmed-article:11679074 | pubmed:articleTitle | Mutation of luxS affects growth and virulence factor expression in Streptococcus pyogenes. | lld:pubmed |
pubmed-article:11679074 | pubmed:affiliation | Department of Molecular Microbiology, Washington University School of Medicine, Box 8230, St Louis, MO 63110-1093, USA. | lld:pubmed |
pubmed-article:11679074 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:11679074 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
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