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PMID:11929534

2016-02-15T04:44:54Z

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'''Sperandio, V, Torres, AG and Kaper, JB''' (2002) Quorum sensing Escherichia coli regulators B and C (QseBC): a novel two-component regulatory system involved in the regulation of flagella and motility by quorum sensing in E. coli. ''Mol. Microbiol.'' '''43''':809-21
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!align=left align='left' bgcolor='#CCCCFF' |Abstract
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Quorum sensing is a cell-to-cell signalling mechanism in which bacteria secrete hormone-like compounds called autoinducers. When these auto-inducers reach a certain threshold concentration, they interact with bacterial transcriptional regulators, thereby regulating gene expression. Enterohaemorrhagic Escherichia coli (EHEC) O157:H7 as well as E. coli K-12 produces the autoinducer-2 (AI-2), which is synthesized by the product of the luxS gene, and previous work from our laboratory has shown that genes encoding the EHEC type III secretion system were activated by quorum sensing. Recently, by hybridizing an E. coli K-12 gene array with cDNA synthesized from RNA extracted from EHEC strain 86-24 and its isogenic luxS mutant, we observed that other potential virulence-associated factors, such as genes encoding the expression and assembly of flagella, motility and chemotaxis, were also activated by quorum sensing. The array data also indicated that several genes encoding putative E. coli regulators were controlled by quorum sensing. In this report, we describe a two-component system regulated by quorum sensing that shares homology with Salmonella typhimurium PmrAB, which we have named quorum sensing E. coli regulator B and C (QseBC). The qseBC genes, previously identified only as open reading frames b3025 and b3026, are organized in an operon in the E. coli chromosome, with qseB encoding the response regulator and qseC the sensor kinase. We confirmed the regulation of qseBC by quorum sensing using qseB::lacZ transcriptional fusions and characterized the phenotypes of an isogenic qseC mutation in EHEC. This mutant expressed less flagellin and had reduced motility compared with the wild-type and complemented strains. Transcription of flhD, fliA, motA and fliC::lacZ fusions was decreased in the qseC mutant, suggesting that qseBC is a transcriptional regulator of flagella genes. A qseC mutant was also generated in E. coli K-12 strain MC1000 that showed the same phenotypes as the EHEC mutant, indicating that qseBC regulates flagella and motility by quorum sensing in both EHEC and K-12. QseBC activates transcription of flhDC, which is the master regulator for the flagella and motility genes and, in the absence of flhD, QseBC failed to activate the transcription of fliA. Motility of a luxS, but not of a qseC, mutant can be restored by providing AI-2 exogenously as preconditioned media, suggesting that the qseC mutant is unable to respond to AI-2. However, QseC has no effect on the expression of other quorum sensing-controlled genes such as those encoding for the type III secretion system. These data indicate that QseBC is one component of the quorum-sensing regulatory cascade in both EHEC and K-12 that is involved in the regulation of flagella and motility genes, but that additional regulators in this cascade remain to be characterized.
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[http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=11929534 PubMed]

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DNA-Binding Proteins/genetics; DNA-Binding Proteins/metabolism; Escherichia coli/physiology; Escherichia coli Proteins/genetics; Escherichia coli Proteins/metabolism; Flagella/physiology; Gene Expression Regulation, Bacterial; Molecular Sequence Data; Mutation; Promoter Regions, Genetic; Regulon; Trans-Activators/genetics; Trans-Activators/metabolism; Transcription, Genetic

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==Main Points of the Paper ==
{{LitSignificance}}

== Materials and Methods Used ==
{{LitMaterials}}

==Phenotype Annotations==
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!|Phenotype of!!Taxon Information!!Genotype Information (if known)!!Condition Information!!OMP ID!!OMP Term Name!!ECO ID!!ECO Term Name!!Notes!!Status

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==Notes==

==References==
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<references/>

[[Category:Publication]]

PMID:3934335

2016-01-29T08:14:26Z

51.255.65.73: Fill PMID: Page!

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'''James, W and Mandelstam, J''' (1985) spoVIC, a new sporulation locus in Bacillus subtilis affecting spore coats, germination and the rate of sporulation. ''J. Gen. Microbiol.'' '''131''':2409-19
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A mutation near cysB on the Bacillus subtilis chromosome marks a new sporulation locus, spoVIC. It causes spores to germinate more slowly than those of the wild-type under all conditions and, from indirect evidence, it does not appear to alter the affinity for the germinant L-alanine. The mutant spores have some deficiency of coat proteins (particularly the alkalisoluble coat protein, Mr = 12 000) and the spore coat layers are disorganized. The mutant strain grows normally and sporulates normally until stage II, after which its sporulation is delayed by about 2 h compared to that of the wild-type. This delay results in the prolonged synthesis of some coat proteins and the late synthesis of others. The abnormal coat may be the cause of the germination deficiency. A double mutant strain carrying the spoVIC610 mutation together with gerE36 sporulates slowly. Its spores have very little coat protein, are sensitive to heat, lysozyme and organic solvents, but germinate as well as the strain carrying the spoVIC mutation alone. The role of the spore coat in germination is discussed in the light of these findings.
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[http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=3934335 PubMed]

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Bacillus subtilis/genetics; Bacillus subtilis/physiology; Bacterial Proteins/analysis; Chromosome Mapping; Electrophoresis, Polyacrylamide Gel; Microscopy, Electron; Mutation; Sigma Factor; Spores, Bacterial/physiology; Spores, Bacterial/ultrastructure; Transcription Factors

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==Main Points of the Paper ==
{{LitSignificance}}

== Materials and Methods Used ==
{{LitMaterials}}

==Phenotype Annotations==
{{AnnotationTableHelp}}
<protect>

{| border="2" cellpadding="4" cellspacing="0" style="margin: 1em 1em 1em 0; border: 1px #aaa solid; border-collapse: collapse;" id="H56ab1f61d0325" class=" tableEdit Phenotype_Table_2"
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!|Phenotype of!!Taxon Information!!Genotype Information (if known)!!Condition Information!!OMP ID!!OMP Term Name!!ECO ID!!ECO Term Name!!Notes!!Status

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|<div class="tableEdit_editLink plainlinks">[{{SERVER}}{{SCRIPTPATH}}?title=Special:TableEdit&id=d41d8cd98f00b204e9800998ecf8427e.7545.H56ab1f61d0325&page=7545&pagename={{FULLPAGENAMEE}}&type=0&template=Phenotype_Table_2 edit table]</div> || || || || || || || || ||
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==Notes==

==References==
{{RefHelp}}
<references/>

[[Category:Publication]]

PMID:3934335

2016-01-29T08:14:23Z

51.255.65.73: New PMID: Page!

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