Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
2000-6-13
pubmed:abstractText
One of the essential features of all pathogenic strains of Salmonella enterica is the ability to enter into nonphagocytic cells. This pathogenic property is mediated by the Salmonella pathogenicity island 1 (SPI-1)-encoded type III secretion system. Expression of components and substrates of this system is subject to complex regulatory mechanisms. These mechanisms include a number of specific and global transcriptional regulatory proteins. In this study we have compared in S. enterica serovars Typhimurium and Typhi the effect of mutations in flagellar genes on the phenotypes associated with the SPI-1 type III protein secretion system. We found that serovar Typhi strains carrying a null mutation in either of the flagellar regulatory genes flhDC or fliA were severely deficient in entry into cultured epithelial cells and macrophage cytotoxicity. This defect could not be reversed by applying a mild centrifugal force, suggesting that the effects of the mutations were not due to the absence of motility. In contrast, the same mutations had no significant effect on the ability of serovar Typhimurium to enter into cultured Henle-407 cells or to induce macrophage cell death. Consistent with these observations, we found that the mutations in the flagellar regulatory proteins significantly reduced the expression of components of the SPI-1-encoded type III system in serovar Typhi but had a marginal effect in serovar Typhimurium. Our results therefore indicate that there is an overlap between regulatory mechanisms that control flagellar and type III secretion gene expression in Salmonella serovar Typhi.
pubmed:grant
pubmed:commentsCorrections
http://linkedlifedata.com/resource/pubmed/commentcorrection/10768967-10047557, http://linkedlifedata.com/resource/pubmed/commentcorrection/10768967-10048039, http://linkedlifedata.com/resource/pubmed/commentcorrection/10768967-10339609, http://linkedlifedata.com/resource/pubmed/commentcorrection/10768967-10411731, http://linkedlifedata.com/resource/pubmed/commentcorrection/10768967-10417179, http://linkedlifedata.com/resource/pubmed/commentcorrection/10768967-1495387, http://linkedlifedata.com/resource/pubmed/commentcorrection/10768967-1587617, http://linkedlifedata.com/resource/pubmed/commentcorrection/10768967-1624429, http://linkedlifedata.com/resource/pubmed/commentcorrection/10768967-1639496, http://linkedlifedata.com/resource/pubmed/commentcorrection/10768967-2077343, http://linkedlifedata.com/resource/pubmed/commentcorrection/10768967-2152887, http://linkedlifedata.com/resource/pubmed/commentcorrection/10768967-2160435, http://linkedlifedata.com/resource/pubmed/commentcorrection/10768967-2349239, http://linkedlifedata.com/resource/pubmed/commentcorrection/10768967-2544889, http://linkedlifedata.com/resource/pubmed/commentcorrection/10768967-2548211, http://linkedlifedata.com/resource/pubmed/commentcorrection/10768967-2680969, http://linkedlifedata.com/resource/pubmed/commentcorrection/10768967-2840399, http://linkedlifedata.com/resource/pubmed/commentcorrection/10768967-569495, http://linkedlifedata.com/resource/pubmed/commentcorrection/10768967-6123543, http://linkedlifedata.com/resource/pubmed/commentcorrection/10768967-6818149, http://linkedlifedata.com/resource/pubmed/commentcorrection/10768967-7015147, http://linkedlifedata.com/resource/pubmed/commentcorrection/10768967-7608068, http://linkedlifedata.com/resource/pubmed/commentcorrection/10768967-7730257, http://linkedlifedata.com/resource/pubmed/commentcorrection/10768967-7752894, http://linkedlifedata.com/resource/pubmed/commentcorrection/10768967-7783646, http://linkedlifedata.com/resource/pubmed/commentcorrection/10768967-7798666, http://linkedlifedata.com/resource/pubmed/commentcorrection/10768967-7997169, http://linkedlifedata.com/resource/pubmed/commentcorrection/10768967-8045880, http://linkedlifedata.com/resource/pubmed/commentcorrection/10768967-8057852, http://linkedlifedata.com/resource/pubmed/commentcorrection/10768967-8206838, http://linkedlifedata.com/resource/pubmed/commentcorrection/10768967-8235660, http://linkedlifedata.com/resource/pubmed/commentcorrection/10768967-8288531, http://linkedlifedata.com/resource/pubmed/commentcorrection/10768967-8514418, http://linkedlifedata.com/resource/pubmed/commentcorrection/10768967-8548821, http://linkedlifedata.com/resource/pubmed/commentcorrection/10768967-8596461, http://linkedlifedata.com/resource/pubmed/commentcorrection/10768967-8631681, http://linkedlifedata.com/resource/pubmed/commentcorrection/10768967-8817493, http://linkedlifedata.com/resource/pubmed/commentcorrection/10768967-8830263, http://linkedlifedata.com/resource/pubmed/commentcorrection/10768967-8885278, http://linkedlifedata.com/resource/pubmed/commentcorrection/10768967-8951818, http://linkedlifedata.com/resource/pubmed/commentcorrection/10768967-9587187, http://linkedlifedata.com/resource/pubmed/commentcorrection/10768967-9723922
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
0019-9567
pubmed:author
pubmed:issnType
Print
pubmed:volume
68
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
2735-43
pubmed:dateRevised
2009-11-18
pubmed:meshHeading
pubmed:year
2000
pubmed:articleTitle
The flagellar sigma factor FliA (sigma(28)) regulates the expression of Salmonella genes associated with the centisome 63 type III secretion system.
pubmed:affiliation
Section of Microbial Pathogenesis, Boyer Center for Molecular Medicine, Yale School of Medicine, New Haven, Connecticut 06536-0812, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.