Locality versus globality in bacterial signalling: can local communication stabilize bacterial communities?
BACKGROUND
Microbial consortia are a major form of life; however their stability conditions are poorly understood and are often explained in terms of species-specific defence mechanisms (secretion of extracellular matrix, antimicrobial compounds, siderophores, etc.). Here we propose a hypothesis that the primarily local nature of intercellular signalling can be a general mechanism underlying the stability of many forms of microbial communities.


OBJECTIVE
We propose that a large microbial community can be pictured as a theatre of spontaneously emerging, partially overlapping, locally recruited microcommunities whose members interact primarily among themselves, via secreted (signalling) molecules or cell-cell contacts. We hypothesize that stability in an open environment relies on a predominantly local steady state of intercellular communication which ensures that i) deleterious mutants or strains can be excluded by a localized collapse, while ii) microcommunities harbouring useful traits can persist and/or spread even in the absence of specific protection mechanisms.


METHODS
Some elements of this model can be tested experimentally by analyzing the behaviour of synthetic consortia composed of strains having well-defined communication systems and devoid of specific defence mechanisms. Supporting evidence can be obtained by in silico simulations.


CONCLUSIONS
The hypothesis provides a framework for a systematic comparison of bacterial community behavior in open and closed environments. The model predicts that local signalling may enable multispecies communities to colonize open, structured environments. On the other hand, a confined niche or a host may be more likely to be colonized by a bacterial mono-species community, and local communication here provides a control against spontaneously arising cheaters, provided that survival depends on cooperation.
Venturi
Vittorio
V
International Centre for Genetic Engineering and Biotechnology, 34012 Trieste, Italy. venturi@icgeb.org
Kerényi
Adám
A
Reiz
Beáta
B
Bihary
Dóra
D
Pongor
Sándor
S
D001419:Bacteria / Q000378:metabolism*; D015964:Gene Expression Regulation, Bacterial / Q000502:physiology*; D008954:Models, Biological; D015398:Signal Transduction / Q000502:physiology*