Abstract
The flagellar apparatus consists of components that function as a type III secretion system (TTSS). Enteropathogenic and enterohaemorrhagic E. coli (EPEC and EHEC, respectively) produce an additional TTSS, which is involved in virulence via the translocation of effector proteins into infected host cells. This system is encoded by the locus of enterocyte effacement (LEE). The authors observed that EPEC and EHEC grown in Dulbecco's modified Eagle's medium to the mid- and late-exponential growth phase at 37 degrees C are non-motile. At the same time these conditions trigger the expression of the LEE-encoded TTSS. Furthermore, it was found that EPEC with an inactivated ihfA, which encodes the IHFalpha subunit of the integration host factor (IHF), becomes hyperflagellated and motile. Similar hypermotility was seen upon inactivation of the ihfA of EHEC strains. IHF-mediated repression of the EPEC flagella involves down-regulation of flhDC, which encodes a positive regulator of the flagellar regulon. IHF indirectly mediates flhDC repression, via a putative EPEC-unique regulator which is not encoded by LEE.
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