Evidence of Cross-Regulation in Two Closely Related Pyruvate-Sensing Systems in
Uropathogenic Escherichia coli.
Authors Steiner BD, Eberly AR, Hurst MN, Zhang EW, Green HD, Behr S, Jung K,
Hadjifrangiskou M
Submitted By Maria Hadjifrangiskou on 2/5/2018
Status Published
Journal The Journal of membrane biology
Year 2018
Date Published 1/27/2018
Volume : Pages Not Specified : Not Specified
PubMed Reference 29374286
Abstract Two-component systems (TCSs) dictate many bacterial responses to environmental
change via the activation of a membrane-embedded sensor kinase, which has
molecular specificity for a cognate response regulator protein. However,
although the majority of TCSs operate through seemingly strict cognate
protein-protein interactions, there have been several reports of TCSs that
violate this classical model of signal transduction. Our group has recently
demonstrated that some of these cross-interacting TCSs function in a manner that
imparts a fitness advantage to bacterial pathogens. In this study, we describe
interconnectivity between the metabolite-sensing TCSs YpdA/YpdB and BtsS/BtsR in
uropathogenic Escherichia coli (UPEC). The YpdA/YpdB and BtsS/BtsR TCSs have
been previously reported to interact in K12 E. coli, where they alter the
expression of putative transporter genes yhjX and yjiY, respectively. These
target genes are both upregulated in UPEC during acute and chronic murine models
of urinary tract infection, as well as in response to pyruvate and serine added
to growth media in vitro. Here, we show that proper regulation of yhjX in UPEC
requires the presence of all components from both of these TCSs. By utilizing
plasmid-encoded luciferase reporters tracking the activity of the yhjX and yjiY
promoters, we demonstrate that deletions in one TCS substantially alter
transcriptional activity of the opposing system's target gene. However, unlike
in K12 E. coli, single gene deletions in the YpdA/YpdB system do not alter yjiY
gene expression in UPEC, suggesting that niche and lifestyle-specific pressures
may be selecting for differential cross-regulation of TCSs in pathogenic and
non-pathogenic E. coli.

Investigators with authorship
Maria HadjifrangiskouVanderbilt University