rdf:type |
|
lifeskim:mentions |
umls-concept:C0040649,
umls-concept:C0314672,
umls-concept:C0445750,
umls-concept:C0871261,
umls-concept:C1145667,
umls-concept:C1167622,
umls-concept:C1301676,
umls-concept:C1513371,
umls-concept:C1515877,
umls-concept:C1704632,
umls-concept:C1704735,
umls-concept:C1706817,
umls-concept:C1879547,
umls-concept:C2349209,
umls-concept:C2825311,
umls-concept:C2911692
|
pubmed:issue |
3
|
pubmed:dateCreated |
2011-1-17
|
pubmed:abstractText |
The response regulator SsrB activates expression of genes encoded within and outside of a pathogenicity island (SPI-2), which is required for systemic infection of Salmonella. SsrB binds upstream of the sifA, sifB, and sseJ effector genes and directly regulates transcription. SsrB also relieves gene silencing by the nucleoid protein H-NS. Single molecule experiments with magnetic tweezers demonstrated that SsrB displaces H-NS from DNA only when it is bound in a polymerization (stiffening) mode and not when H-NS is bound to DNA in the bridging mode. Thus, in contrast to previous views, the polymerization binding mode of H-NS is the relevant form for counter-silencing by SsrB. Our results reveal that response regulators can directly activate transcription and also relieve H-NS silencing. This study adds to the repertoire of mechanisms by which NarL/FixJ subfamily members regulate transcription. Because SsrB-dependent promoters are diversely organized, additional mechanisms of transcriptional activation at other loci are likely.
|
pubmed:grant |
|
pubmed:language |
eng
|
pubmed:journal |
|
pubmed:citationSubset |
IM
|
pubmed:chemical |
|
pubmed:status |
MEDLINE
|
pubmed:month |
Jan
|
pubmed:issn |
1083-351X
|
pubmed:author |
|
pubmed:issnType |
Electronic
|
pubmed:day |
21
|
pubmed:volume |
286
|
pubmed:owner |
NLM
|
pubmed:authorsComplete |
Y
|
pubmed:pagination |
1895-902
|
pubmed:meshHeading |
pubmed-meshheading:21059643-Bacterial Proteins,
pubmed-meshheading:21059643-DNA, Bacterial,
pubmed-meshheading:21059643-DNA-Binding Proteins,
pubmed-meshheading:21059643-Gene Expression Regulation, Bacterial,
pubmed-meshheading:21059643-Gene Silencing,
pubmed-meshheading:21059643-Genetic Loci,
pubmed-meshheading:21059643-Glycoproteins,
pubmed-meshheading:21059643-Salmonella enterica,
pubmed-meshheading:21059643-Transcription, Genetic,
pubmed-meshheading:21059643-Transcription Factors
|
pubmed:year |
2011
|
pubmed:articleTitle |
Salmonella enterica response regulator SsrB relieves H-NS silencing by displacing H-NS bound in polymerization mode and directly activates transcription.
|
pubmed:affiliation |
Department of Microbiology and Immunology, University of Illinois, Chicago, Illinois 60612, USA.
|
pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, Non-P.H.S.,
Research Support, Non-U.S. Gov't,
Research Support, N.I.H., Extramural
|