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. Author manuscript; available in PMC: 2016 Sep 9.
Published in final edited form as: Cell Host Microbe. 2015 Sep 9;18(3):275–284. doi: 10.1016/j.chom.2015.08.007

Fig. 3.

Fig. 3

Adrenergic and nutrient signals intersect to control expression of the EHEC LEE. Host hormones Epinephrine (Epi) and Norepinephrine (NE), whose intestinal availability is modulated by the microbiota, are recognized by two sensor histidine kinases, QseC and QseE. QseC also recognizes the microbiota-derived quorum sensing molecule AI-3. QseC and QseE phosphorylate their cognate response regulators (RR) QseB and QseE respectively and QseC also phosphorylates RRs KdpE and QseF. KdpE interacts with the master regulator of carbon metabolism Cra to activate Ler, which Cra also activates under gluconeogenic conditions (ex: low glucose levels, high levels of succinate). The mucosal sugar fucose, whose liberation is microbiota dependent, is recognized by another HK FusK. FusR, the cognate RR of FusK, represses activation of the LEE. Expression of FusKR is repressed by the QseC/QseE signalling cascade.