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. 2020 Oct 29;16(10):e1008934.
doi: 10.1371/journal.ppat.1008934. eCollection 2020 Oct.

Dual-function quorum-sensing systems in bacterial pathogens and symbionts

Affiliations

Dual-function quorum-sensing systems in bacterial pathogens and symbionts

Kelsey Barrasso et al. PLoS Pathog. .
No abstract available

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Conflict of interest statement

The authors have declared that no competing interests exist.

Figures

Fig 1
Fig 1. The AI-3/Epi/NE signaling pathway in EHEC.
The HK QseC detects Epi and NE made by the host, as well as AI-3 produced by the EHEC enzyme TDH. Binding of these molecules to the HK enables QseC to control the activity of the 3 RRs KdpE, QseB, and QseF, which results in regulation of downstream virulence genes. AI-3, autoinducer-3; EHEC, enterohemorrhagic Escherichia coli O157:H7; Epi, epinephrine; HK, histidine kinase; NE, norepinephrine; RRs, response regulator; TDH, threonine dehydrogenase. Created with BioRender.com.
Fig 2
Fig 2. Vibrio signaling pathways for QS and host sensing.
Various HK receptors in Vibrio species recognize distinct signals produced by the bacterium (sensing “self”) and/or produced by host cells or neighboring bacteria (sensing “other”). The conservation of the HKs varies among species, and this figure indicates the proteins and signals determined in the literature for each species (V.h, Vibrio harveyi; V.c., Vibrio cholerae; V.p., Vibrio parahaemolyticus; V.f., Vibrio fischeri). Signals produced by enzymes (if known) are indicated for each system. In the absence of cognate signals, phosphorylation (P) of LuxU and LuxO leads to production of AphA and low production of LuxR (V.h.)/HapR (V.c.)/OpaR (V.p.)/LitR (V.f.) and expression of biofilm, virulence, and type III secretion genes. In the presence of signals, dephosphorylation of LuxU drives production of LuxR/HapR/OpaR/LitR and expression of bioluminescence, proteases, and type VI secretion genes. The NO/H-NOX/HahK pathway in V.f. inhibits syp gene expression and biofilm formation. The VqmA/DPO pathway inhibits biofilm formation in V.c. AI-2, autoinducer-2; CAI-1, cholera autoinducer-1; CP, cytoplasm; DPO, 3,5-dimethyl-pyrazin-2-ol; HAI-1, harveyi autoinducer-1; HK, histidine kinase; H-NOX, heme nitric oxide/oxygen binding; NO, nitric oxide; PP, periplasm; QS, quorum sensing. Created with BioRender.com.

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