Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2001-8-7
pubmed:databankReference
pubmed:abstractText
Production of curli (AgF) adhesins by Escherichia coli and Salmonella enterica serovar Typhimurium (S. typhimurium) is associated with extracellular matrix production and is optimal at low temperature during stationary phase. Curli and extracellular matrix synthesis involves a complex regulatory network that is dependent on the CsgD (AgfD) regulator. We have identified a novel regulator, termed MlrA, that is required for curli production and extracellular matrix formation. Two cosmids from a genomic library of avian pathogenic E. coli chi7122 conferred mannose-resistant haemagglutination (HA) and curli production to E. coli HB101, which is unable to produce curli owing to a defective regulatory pathway. The rpoS gene, encoding a known positive regulator of curli synthesis, and the E. coli open reading frame (ORF) of unknown function, yehV, identified on each of these cosmids, respectively, conferred curli production and HA to E. coli HB101. We have designated yehV as the mlrA gene for MerR-like regulator A because its product shares similarities with regulatory proteins of the MerR family. HA and curli production by strain chi7122 were abolished by disruption of rpoS, mlrA or csgA, the curli subunit gene. Both csgD and csgBA transcription, required for expression of curli, were inactive in an mlrA mutant grown under conditions that promote curli production. An mlrA homologue was identified in S. typhimurium. Analysis of mlrA-lac operon fusions demonstrated that mlrA was positively regulated by rpoS. mlrA mutants of wild-type S. typhimurium SL1344 or SR-11 no longer produced curli or rugose colony morphology, and exhibited enhanced aggregation and extracellular matrix formation when complemented with the mlrA gene from either S. typhimurium or E. coli present on a low-copy-number plasmid. However, inactivation of mlrA did not affect curli production and aggregative morphology in an upregulated curli producing S. typhimurium derivative containing a temperature- and RpoS-independent agfD promoter region. These results indicate that MlrA is a newly defined transcriptional regulator of csgD/agfD that acts as a positive regulator of RpoS-dependent curli and extracellular matrix production by E. coli and S. typhimurium.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
0950-382X
pubmed:author
pubmed:issnType
Print
pubmed:volume
41
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
349-63
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed-meshheading:11489123-Adhesins, Bacterial, pubmed-meshheading:11489123-Amino Acid Sequence, pubmed-meshheading:11489123-Animals, pubmed-meshheading:11489123-Bacterial Proteins, pubmed-meshheading:11489123-Chickens, pubmed-meshheading:11489123-Cloning, Molecular, pubmed-meshheading:11489123-DNA, Bacterial, pubmed-meshheading:11489123-Escherichia coli, pubmed-meshheading:11489123-Escherichia coli Proteins, pubmed-meshheading:11489123-Extracellular Matrix, pubmed-meshheading:11489123-Fimbriae, Bacterial, pubmed-meshheading:11489123-Gene Expression Regulation, Bacterial, pubmed-meshheading:11489123-Genes, Bacterial, pubmed-meshheading:11489123-Genes, Regulator, pubmed-meshheading:11489123-Genes, Reporter, pubmed-meshheading:11489123-Genetic Complementation Test, pubmed-meshheading:11489123-Hemagglutination, pubmed-meshheading:11489123-Molecular Sequence Data, pubmed-meshheading:11489123-Open Reading Frames, pubmed-meshheading:11489123-Salmonella typhimurium, pubmed-meshheading:11489123-Sigma Factor
pubmed:year
2001
pubmed:articleTitle
MlrA, a novel regulator of curli (AgF) and extracellular matrix synthesis by Escherichia coli and Salmonella enterica serovar Typhimurium.
pubmed:affiliation
Department of Biology, Washington University, Saint Louis, MO 63130-2525, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, U.S. Gov't, Non-P.H.S., Research Support, Non-U.S. Gov't