The fim switch in Escherichia coli is the mechanism by which the fim gene cluster, encoding Type I Pili,[1] is transcriptionally controlled.
These pili are virulence factors involved in adhesion, especially important in uropathogenic Escherichia coli. The gene undergoes phase variation mediated via two recombinases and is a model example of site specific inversion.
The operon consists of the promoter region fim S, the main constituent fim A, its gene product forming a rod like structure and fim H, coding for an adhesin at the tip, to name just a few important elements. The fim S region is flanked by 9bp repeats that are mirror images of each other.[2] These mirror images serve as substrates for two ATP-dependent recombinases, fim B and fim E. These recombinases can invert the orientation of the fim S region and only one orientation allows for 3' to 5' transcription.
fim B "flips" the promoter region both ways, from the "on" position to the "off" position and vice versa, whereas fim E can only facilitate recombination from "on" to "off". This equilibrium, shifted towards maintaining the "off" position, due to higher fim E activity,[3] serves as a mode of expressing pili only when adhesion is needed. Another level of transcriptional control in E. coli is mediated by the sensitivity of the recombinases to pH and osmolarity,[4] further ensuring appropriate expression levels of type-I pili, given the stark differences in osmolarity inside and outside an animal's body. Type-I pili are expressed by many species of Enterobacteriaceae. The transcriptional control can differ widely between species,[5] in Salmonella typhimurium, for example much influence is exerted by a leucine-responsive regulatory protein and there is no fim S element.