M. Falconi et al., Involvement of FIS in the H-NS-mediated regulation of virF gene of Shigella and enteroinvasive Escherichia coli, MOL MICROB, 42(2), 2001, pp. 439-452
The mechanism of pathogenicity in Shigella and enteroinvasive Escherichia c
oli (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 tota
lly restored when Shigella wildtype fis gene is offered in trans. We also i
dentified virF, among the virulence genes, as a target of FIS-mediated acti
vation and showed that FIS binds to four specific sites in the promoter reg
ion of virF. Previous studies have demonstrated that the expression of VirF
, the first positive activator of a multistep regulatory cascade, is subjec
t to temperature-dependent regulation by H-NS, one of the main nucleoid-ass
ociated 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 perm
issive temperature (37 degreesC), when H-NS fails to repress virF, as well
as an indirect effect by partially counteracting H-NS inhibition at the tra
nsition temperature (32 degreesC). Our data indicate that FIS may be releva
nt for the rapid increase in virF expression after penetration of bacteria
into the host.