SummaryThe mechanism of pathogenicity in Shigella and enteroinvasive Escherichia coli (EIEC) requires the co-ordinated expression of several genes located on both the virulence plasmid and the chromosome. We found that cells lacking a functional FIS protein (factor for inversion stimulation) are partially impaired in expressing the virulence genes and that full expression is totally restored when Shigella wildtype fis gene is offered in trans. We also identified virF, among the virulence genes, as a target of FISmediated activation and showed that FIS binds to four specific sites in the promoter region of virF. Previous studies have demonstrated that the expression of VirF, the first positive activator of a multistep regulatory cascade, is subject to temperature-dependent regulation by H-NS, one of the main nucleoidassociated proteins. We now demonstrate that two of the four FIS sites overlap one of the two H-NS sites responsible for thermoregulation (H-NS site I). FIS was found to exercise a direct positive transcriptional control at permissive temperature (378C), when H-NS fails to repress virF, as well as an indirect effect by partially counteracting H-NS inhibition at the transition temperature (328C). Our data indicate that FIS may be relevant for the rapid increase in virF expression after penetration of bacteria into the host.

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