Expression of virulence factors in non-typhoidal
Salmonella enterica
depends on a wide variety of general and specific transcriptional factors that act in response to multiple environmental signals. Expression of genes for cellular invasion located in the
Salmonella
pathogenicity island 1 (SPI-1) is tightly regulated by several transcriptional regulators arrayed in a cascade, while repression of this system is exerted mainly by H-NS. In SPI-1, H-NS represses the expression mainly by binding to the regulatory region of
hilA
and derepression is exercised mainly by HilD. However, the possible regulatory role of H-NS in genes downstream from HilD and HilA, such as those regulated by InvF, has not been fully explored. Here the role of H-NS on the expression of
sopB
, an InvF dependent gene encoded in SPI-5, was evaluated. Our data show that InvF is required for the expression of
sopB
even in the absence of H-NS. Furthermore, in agreement with previous results on other InvF-regulated genes, we found that the expression of
sopB
requires the InvF/SicA complex. Our results support that SicA is not required for DNA binding nor for increasing affinity of InvF to DNA
in vitro
. Moreover, by using a bacterial two-hybrid system we were able to identify interactions between SicA and InvF. Lastly, protein-protein interaction assays suggest that InvF functions as a monomer. Derived from these results we postulate that the InvF/SicA complex does not act on
sopB
as an anti-H-NS factor; instead, it seems to induce the expression of
sopB
by acting as a classical transcriptional regulator.