The σ^S(or RpoS) subunit of RNA polymerase is the master regulator of the general stress response inEscherichia coli. While nearly absent in rapidly growing cells, σ^Sis strongly induced during entry into stationary phase and/or many other stress conditions and is essential for the expression of multiple stress resistances. Genome-wide expression profiling data presented here indicate that up to 10% of theE. coligenes are under direct or indirect control of σ^Sand that σ^Sshould be considered a second vegetative sigma factor with a major impact not only on stress tolerance but on the entire cell physiology under nonoptimal growth conditions. This large data set allowed us to unequivocally identify a σ^Sconsensus promoter in silico. Moreover, our results suggest that σ^S-dependent genes represent a regulatory network with complex internal control (as exemplified by the acid resistance genes). This network also exhibits extensive regulatory overlaps with other global regulons (e.g., the cyclic AMP receptor protein regulon). In addition, the global regulatory protein Lrp was found to affect σ^Sand/or σ⁷⁰selectivity of many promoters. These observations indicate that certain modules of the σ^S-dependent general stress response can be temporarily recruited by stress-specific regulons, which are controlled by other stress-responsive regulators that act together with σ⁷⁰RNA polymerase. Thus, not only the expression of genes within a regulatory network but also the architecture of the network itself can be subject to regulation.

Type 1 fimbriae ofEscherichia colifacilitate attachment to the host mucosa and promote biofilm formation on abiotic surfaces. The transcriptional regulator LrhA, which is known as a repressor of flagellar, motility and chemotaxis genes, regulates biofilm formation and expression of type 1 fimbriae. Whole-genome expression profiling revealed that inactivation oflrhAresults in an increased expression of structural components of type 1 fimbriae.In vitro, LrhA bound to the promoter regions of the twofimrecombinases (FimB and FimE) that catalyse the inversion of thefimApromoter, and to the invertible element itself. TranslationallacZfusions with these genes and quantification offimEtranscript levels by real-time PCR showed that LrhA influences type 1 fimbrial phase variation, primarily via activation of FimE, which is required for the ON-to-OFF transition of thefimswitch. Enhanced type 1 fimbrial expression as a result oflrhAdisruption was confirmed by mannose-sensitive agglutination of yeast cells. Biofilm formation was stimulated bylrhAinactivation and completely suppressed upon LrhA overproduction. The effects of LrhA on biofilm formation were exerted via the changed levels of surface molecules, most probably both flagella and type 1 fimbriae. Together, the data show a role for LrhA as a repressor of type 1 fimbrial expression, and thus as a regulator of the initial stages of biofilm development and, presumably, bacterial adherence to epithelial host cells also.