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Zusammenfassung: <jats:title>ABSTRACT</jats:title> <jats:p> In order to survive inside macrophages, <jats:named-content content-type="genus-species">Salmonella</jats:named-content> produces a series of proteins encoded by genes within <jats:named-content content-type="genus-species">Salmonella</jats:named-content> pathogenicity island 2 (SPI-2). In the present study, we report that Fur, a central regulator of iron utilization, negatively controls the expression of SPI-2 genes. Time course analysis of SPI-2 expression after the entry of <jats:named-content content-type="genus-species">Salmonella</jats:named-content> into macrophages revealed that SPI-2 genes are induced earlier and at higher levels in the absence of the Fur regulator. It was hypothesized that Fur repressed the SPI-2 expression that was activated during acidification of the phagosome. Indeed, as pH was lowered from pH 7.0 to pH 5.5, the lack of Fur enabled SPI-2 gene expression to be induced at higher pH and to be expressed at higher levels. Fur controlled SPI-2 genes via repression of the SsrB response regulator, a primary activator of SPI-2 expression. Fur repressed <jats:italic>ssrB</jats:italic> expression both inside macrophages and under acidic conditions, which we ascribe to the direct binding of Fur to the <jats:italic>ssrB</jats:italic> promoter. Our study suggests that <jats:named-content content-type="genus-species">Salmonella</jats:named-content> could employ iron inside the phagosome to precisely control the timing and levels of SPI-2 expression inside macrophages. </jats:p>
Umfang: 2203-2210
ISSN: 0019-9567
1098-5522
DOI: 10.1128/iai.01625-13