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dc.contributor.authorK. Coombes, Brianen_US
dc.contributor.authorF. Brown, Naten_US
dc.contributor.authorVandez, Yaneten_US
dc.contributor.authorH. Brumell, Johnen_US
dc.contributor.authorBrett Finlay, B.en_US
dc.date.accessioned2017-04-24T09:23:19Z
dc.date.available2017-04-24T09:23:19Z
dc.date.issued2004en_US
dc.date.modified2008-11-19T02:55:22Z
dc.identifier.issn00219258en_US
dc.identifier.doi10.1074/jbc.M404299200en_AU
dc.identifier.urihttp://hdl.handle.net/10072/15338
dc.description.abstractSalmonella pathogenicity island (SPI)-2 is pivotal to the intracellular survival of Salmonella and for virulence in mammals. SPI-2 encodes virulence factors (called effectors) that are translocated into the host cell, a type III secretion apparatus and a two-component regulatory system that regulates intracellular expression of SPI-2. Salmonella SPI-2 secretion activity appears to be induced in response to acidification of the vacuole in which it replicates. Here we show that the expression of the SPI-2 proteins, SseB and SseD (filament and pore forming components of the secretion apparatus, respectively) in response to acidification requires an intact secretion system and SsaL, a Salmonella homologue of SepL, a regulator required for type III-dependent secretion of translocators but not effectors in attaching and effacing gastrointestinal pathogens. We show that the expression of SPI-2-encoded effectors is acid-regulated but can be uncoupled from the expression of filament and translocon components, thus showing a differential requirement of SsaL for expression. The secretion and translocation of SPI-2-encoded effectors requires SsaL, but SsaL is dispensable for the secretion of SPI-2 effectors encoded in other pathogenicity loci, suggesting a secretion regulation function for SsaL. Further, we demonstrate that the differential expression of adjacent genes within the sseA operon (sseD and sseE) occurs at the transcriptional level. These data indicate that a Salmonella SPI-2 activation state is achieved by an acidregulated response that requires SsaL. These data also suggest the existence of a previously unrecognized regulatory element within SPI-2 for the "effector operon" region downstream of sseD that might demarcate the expression of translocators and effectors.en_US
dc.description.peerreviewedYesen_US
dc.description.publicationstatusYesen_AU
dc.languageEnglishen_US
dc.language.isoen_AU
dc.publisherAmerican Society for Biochemistry and Molecular Biologyen_US
dc.publisher.placeUSAen_US
dc.publisher.urihttp://www.jbc.org/en_AU
dc.relation.ispartofpagefrom49804en_US
dc.relation.ispartofpageto49815en_US
dc.relation.ispartofissue48en_US
dc.relation.ispartofjournalJournal of Biological Chemistryen_US
dc.relation.ispartofvolume279en_US
dc.subject.fieldofresearchcode270103en_US
dc.subject.fieldofresearchcode270304en_US
dc.titleExpression and secretion of Salmonella pathogenicity island-2 virulence genes in response to acidification exhibit differential requirements of a functional type III secretion apparatus and SsaLen_US
dc.typeJournal articleen_US
dc.type.descriptionC1 - Peer Reviewed (HERDC)en_US
dc.type.codeC - Journal Articlesen_US
gro.date.issued2004
gro.hasfulltextNo Full Text


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