title: The LysR-type transcriptional regulator QseD alters type three secretion in enterohemorrhagic Escherichia coli and motility in K-12 Escherichia coli.
abstract: Enterohemorrhagic Escherichia coli (EHEC) O157:H7 responds to the host-produced epinephrine and norepinephrine, and bacterially produced autoinducer 3 (AI-3), through two-component systems. Further integration of multiple regulatory signaling networks, involving regulators such as the LysR-type transcriptional regulator (LTTR) QseA, promotes effective regulation of virulence factors. These include the production of flagella, a phage-encoded Shiga toxin, and genes within the locus of enterocyte effacement (LEE) responsible for attaching and effacing (AE) lesion formation. Here, we describe a new member of this signaling cascade, an LTTR heretofore renamed QseD (quorum-sensing E. coli regulator D). QseD is present in all enterobacteria but exists almost exclusively in O157:H7 isolates as a helix-turn-helix (HTH) truncated isoform. This "short" isoform (sQseD) is still able to regulate gene expression through a different mechanism than the full-length K-12 E. coli "long" QseD isoform (lQseD). The EHEC Delta qseD mutant exhibits increased expression of all LEE operons and deregulation of AE lesion formation. The loss of qseD in EHEC does not affect motility, but the K-12 Delta qseD mutant is hypermotile. While the lQseD directly binds to the ler promoter, encoding the LEE master regulator, to repress LEE transcription, the sQseD isoform does not. LTTRs bind to DNA as tetramers, and these data suggest that sQseD regulates ler by forming heterotetramers with another LTTR. The LTTRs known to regulate LEE transcription, QseA and LrhA, do not interact with sQseD, suggesting that sQseD acts as a dominant-negative partner with a yet-unidentified LTTR.
authors.affiliation: University of Texas Southwestern Medical Center, Department of Microbiology, 5323 Harry Hines Blvd., Dallas, TX 75390-9048, USA.
authors.forename: Benjamin J
authors.initials: BJ
authors.lastname: Habdas
authors.forename: Jennifer
authors.initials: J
authors.lastname: Smart
authors.forename: James B
authors.initials: JB
authors.lastname: Kaper
authors.forename: Vanessa
authors.initials: V
authors.lastname: Sperandio
mesh_terms: D054324:Enterohemorrhagic Escherichia coli / Q000235:genetics / Q000502:physiology*; D048168:Escherichia coli K12 / Q000235:genetics / Q000502:physiology*; D029968:Escherichia coli Proteins / Q000235:genetics / Q000378:metabolism*; D015964:Gene Expression Regulation, Bacterial / Q000502:physiology*; D053038:Quorum Sensing; D012097:Repressor Proteins / Q000235:genetics / Q000378:metabolism*; D012441:Saccharomyces cerevisiae; D014158:Transcription, Genetic
chemical_list: D029968:Escherichia coli Proteins; C550912:HypT protein, E coli; D012097:Repressor Proteins