Article in ISME Journal

Quorum sensing-regulated chitin metabolism provides grazing resistance to Vibrio cholerae biofilms

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Eukaryote ecology has a rich body of established theory that is proving increasingly applicable to biofilm systems as microbial ecologists are taking advantage of the conceptual frameworks long established in ecology theory.

The concepts derived from the study of the interactions of higher organisms can provide a valuable tool for deciphering microbial interactions and begin to bridge the a gap in our understanding of ecologically relevant interactions within environmental biofilm communities.

One such example of the benefits derived from linking a biofilm system with eukarote ecology theory is Sun et al 2015. Here we provide a mechanistic explanation for the adaptive advantage of surface associated growth of Vibrio cholerae in the environment.

Vibrio cholerae is a natural inhabitant of the marine environment and its primary niche is the chitinous surfaces of zooplankton, especially copepods. V. cholerae can utilise chitin as a sole nutrient source and will up-regulate genes involved in horizontal gene transfer (HGT) when attached to chitin, making this niche an important one for acquisition of new genetic material.

Protozoa are a major mortality force for bacteria in the environment and because of this, bacteria have evolved many defence mechanisms. We have shown that for V. cholerae, biofilm formation is one of the protective mechanisms that allows cells to escape grazing pressure from predators such as the cosmopolitan surface feeder, Rhynchomonas nasuta (1).

This study shows that chitin metabolism is regulated by cell to cell communication, or quorum sensing (QS), and further elucidates a role for chitin metabolism in protection from predation by heterotrophic protists or protozoa (2). V. cholerae grown on chitinous surfaces and on Artemia are more toxic to the predator than biofilms grown on abiotic surfaces (plastic or glass). When the gene encoding the QS regulator, hapR was mutated, the chitin-grown biofilms were significantly less toxic. This toxicity was linked to the production of ammonia as a by-product of chitin catabolism.

The fact that biofilms of V. cholerae on chitinous surfaces are better protected than biofilms on abiotic surfaces may explain the adaptive advantage of attachment of V. cholerae to copepods.

This study demonstrates that biofilms can exhibit inducible defences that are due inpart to chemical cues released by the grazer. Further, the factors responsible for virulence may have evolved for some purpose other than virulence to host. As such virulence is a result of selection acting on the pathogen in a different environmental niche, thus supporting the coincidental evolution hypothesis.

1). Matz, C, D McDougald, AM Moreno, PY Yung, FH Yildiz, S Kjelleberg. 2005. Biofilm formation and phenotypic variation enhance predation-driven persistence of Vibrio cholerae. Proc Natl Acad Sci, USA 102:16819-16824.

2) Sun, S, QXM Tay, S Kjellberg, SA Rice, D McDougald. 2015. Quorum sensing-regulated chitin metabolism provides grazing resistance to Vibrio cholerae biofilms. ISME J. 9: 1812–1820

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Diane McDougald

Associate Professor, Singapore Centre for Environmental Life Sciences Engineering

Asst. Prof. McDougald has made significant contributions to the fields of Vibrio biology, bacterial adaptation to stress and mechanisms of molecular control of these responses, cell-to-cell communication, biofilm formation and interactions of bacteria with higher eukaryotes. Her group’s major research interest is on the investigation of mechanisms of survival and persistence of pathogens in the environment, and what impact these mechanisms have on virulence and pathogenicity in the host. They investigate the evolutionary drivers and consequences of bacterial adaptation to stresses, including interactions with higher organisms. Broadly, they study the interactions of prokaryotes and eukaryotes using a number of model systems to investigate the impact of predation by protozoa on microbial communities and how evolution of grazing defences drives the evolution of pathogenicity in the environment. Predation is an important selection pressure that pathogens face in the environment, and as a result, pathogens may evolve phenotypes that not only increase their fitness in the environment, but may also increase their fitness in the human host. This research platform will allow her group to test key aspects of the Coincidental Selection Hypothesis, which states that the virulence of many opportunistic human pathogens may be an accidental by-product of selection for adaptations not related to human disease.


Go to the profile of Jen Thoroughgood
almost 7 years ago
Thanks for sharing this paper Diane.