Article

Spontaneous Gac Mutants of Pseudomonas Biological Control Strains: Cheaters or Mutualists?

Department of Ecology and Evolutionary Biology, University of Arizona, Tucson, Arizona, USA.
Applied and Environmental Microbiology (Impact Factor: 3.67). 08/2011; 77(20):7227-35. DOI: 10.1128/AEM.00679-11
Source: PubMed

ABSTRACT

Bacteria rely on a range of extracellular metabolites to suppress competitors, gain access to resources, and exploit plant or animal hosts. The GacS/GacA two-component regulatory system positively controls the expression of many of these beneficial external products in pseudomonad bacteria. Natural populations often contain variants with defective Gac systems that do not produce most external products. These mutants benefit from a decreased metabolic load but do not appear to displace the wild type in nature. How could natural selection maintain the wild type in the presence of a mutant with enhanced growth? One hypothesis is that Gac mutants are "cheaters" that do not contribute to the public good, favored within groups but selected against between groups, as groups containing more mutants lose access to ecologically important external products. An alternative hypothesis is that Gac mutants have a mutualistic interaction with the wild type, so that each variant benefits by the presence of the other. In the biocontrol bacterium Pseudomonas chlororaphis strain 30-84, Gac mutants do not produce phenazines, which suppress competitor growth and are critical for biofilm formation. Here, we test the predictions of these alternative hypotheses by quantifying interactions between the wild type and the phenazine- and biofilm-deficient Gac mutant within growing biofilms. We find evidence that the wild type and Gac mutants interact mutualistically in the biofilm context, whereas a phenazine-defective structural mutant does not. Our results suggest that the persistence of alternative Gac phenotypes may be due to the stabilizing role of local mutualistic interactions.

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    • "For example , loss-of-function mutations of global regulators gacA and gacS arise at high rates in the laboratory and in natural populations (Duffy and Défago 2000;van den Broek et al. 2005;Driscoll et al. 2011;Seaton et al. 2013). These mutations can confer significant fitness benefits (Duffy and Défago 2000;Driscoll et al. 2011), and lead to loss of public goods, including extracellular enzymes, antibiotics, and biofilm formation (Bull et al. 2001;Seaton et al. 2013), but also private goods involved in primary metabolism (Wei et al. 2013). Similarly, mutations in a LysR-type regulator in Pseudomonas aureofaciens lead to an inability to produce antifungal compounds (Silby et al. 2005). "
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