Integration host factor (IHF) mediates repression of flagella in enteropathogenic and enterohaemorrhagic Escherichia coli

Chen Yona-Nadler, Tatiania Umanski, Shin Ichi Aizawa, Devorah Friedberg, Ilan Rosenshine*

*Corresponding author for this work

Research output: Contribution to journalReview articlepeer-review

49 Scopus citations

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°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 IHFα 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.

Original languageAmerican English
Pages (from-to)877-884
Number of pages8
JournalMicrobiology
Volume149
Issue number4
DOIs
StatePublished - 1 Apr 2003

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