TY - JOUR
T1 - Local and global consequences of flow on bacterial quorum sensing
AU - Kim, Minyoung Kevin
AU - Ingremeau, François
AU - Zhao, Aishan
AU - Bassler, Bonnie Lynn
AU - Stone, Howard A.
N1 - Funding Information:
This work was supported by National Science Foundation grants MCB-1119232 (B.L.B. and H.A.S.) and MCB-1344191 (B.L.B. and H.A.S), the Howard Hughes Medical Institute (B.L.B.), National Institutes of Health grant R01GM065859 (B.L.B.) and an STX fellowship (M.K.K.).
Publisher Copyright:
© 2016 Macmillan Publishers Limited. All rights reserved.
PY - 2016/1/11
Y1 - 2016/1/11
N2 - Bacteria use a chemical communication process called quorum sensing (QS) to control collective behaviours such as pathogenesis and biofilm formation1,2. QS relies on the production, release and group-wide detection of signal molecules called autoinducers. To date, studies of bacterial pathogenesis in well-mixed cultures have revealed virulence factors and the regulatory circuits controlling them, including the overarching role of QS3. Although flow is ubiquitous to nearly all living systems 4, much less explored is how QS influences pathogenic traits in scenarios that mimic host environments, for example, under fluid flow and in complex geometries. Previous studies5-7 have shown that sufficiently strong flow represses QS. Nonetheless, it is not known how QS functions under constant or intermittent flow, how it varies within biofilms or as a function of position along a confined flow, or how surface topography (grooves, crevices, pores) influence QS-mediated communication. We explore these questions using two common pathogens, Staphylococcus aureus and Vibrio cholerae. We identify conditions where flow represses QS and other conditions where QS is activated despite flow, including characterizing geometric and topographic features that influence the QS response. Our studies highlight that, under flow, genetically identical cells do not exhibit phenotypic uniformity with respect to QS in space and time, leading to complex patterns of pathogenesis and colonization. Understanding the ramifications of spatially and temporally non-uniform QS responses in realistic environments will be crucial for successful deployment of synthetic pro- and anti-QS strategies.
AB - Bacteria use a chemical communication process called quorum sensing (QS) to control collective behaviours such as pathogenesis and biofilm formation1,2. QS relies on the production, release and group-wide detection of signal molecules called autoinducers. To date, studies of bacterial pathogenesis in well-mixed cultures have revealed virulence factors and the regulatory circuits controlling them, including the overarching role of QS3. Although flow is ubiquitous to nearly all living systems 4, much less explored is how QS influences pathogenic traits in scenarios that mimic host environments, for example, under fluid flow and in complex geometries. Previous studies5-7 have shown that sufficiently strong flow represses QS. Nonetheless, it is not known how QS functions under constant or intermittent flow, how it varies within biofilms or as a function of position along a confined flow, or how surface topography (grooves, crevices, pores) influence QS-mediated communication. We explore these questions using two common pathogens, Staphylococcus aureus and Vibrio cholerae. We identify conditions where flow represses QS and other conditions where QS is activated despite flow, including characterizing geometric and topographic features that influence the QS response. Our studies highlight that, under flow, genetically identical cells do not exhibit phenotypic uniformity with respect to QS in space and time, leading to complex patterns of pathogenesis and colonization. Understanding the ramifications of spatially and temporally non-uniform QS responses in realistic environments will be crucial for successful deployment of synthetic pro- and anti-QS strategies.
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U2 - 10.1038/nmicrobiol.2015.5
DO - 10.1038/nmicrobiol.2015.5
M3 - Article
C2 - 27571752
AN - SCOPUS:84954564837
SN - 2058-5276
VL - 1
JO - Nature Microbiology
JF - Nature Microbiology
IS - 1
M1 - 15005
ER -