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Phenotypic plasticity in prey can have a dramatic impact on predator-prey dynamics, e.g. by inducible defense against temporally varying levels of predation. Previous work has overwhelmingly shown that this effect is stabilizing: inducible defenses dampen the amplitudes of population oscillations or eliminate them altogether. However, such studies have neglected scenarios where being protected against one predator increases vulnerability to another (incompatible defense). Here we develop a model for such a scenario, using two distinct prey phenotypes and two predator species. Each prey phenotype is defended against one of the predators, and vulnerable to the other. In strong contrast with previous studies on the dynamic effects of plasticity involving a single predator, we find that increasing the level of plasticity consistently destabilizes the system, as measured by the amplitude of oscillations and the coefficients of variation of both total prey and total predator biomasses. We explain this unexpected and seemingly counterintuitive result by showing that plasticity causes synchronization between the two prey phenotypes (and, through this, between the predators), thus increasing the temporal variability in biomass dynamics. These results challenge the common view that plasticity should always have a stabilizing effect on biomass dynamics: adding a single predator-prey interaction to an established model structure gives rise to a system where different mechanisms may be at play, leading to dramatically different outcomes.
Biofilm formation in bacteria is considered to be one strategy to avoid protozoan grazing. However, this assumption is largely based on experiments with suspension-feeding protozoans. Here we test the hypothesis that grazing resistance depends on both the grazers’ feeding trait and the bacterial phenotype, rather than being a general characteristic of bacterial biofilms. We combined batch experiments with mathematical modelling, considering the bacterium Pseudomonas putida and either a suspension-feeding (i.e. the ciliate Paramecium tetraurelia) or a surface-feeding grazer (i.e. the amoeba Acanthamoeba castellanii). We find that both plankton and biofilm phenotypes were consumed, when exposed to their specialised grazer, whereas the other phenotype remained grazing-resistant. This was consistently shown in two experiments (starting with either only planktonic bacteria or with additional pre-grown biofilms) and matches model predictions. In the experiments, the plankton feeder strongly stimulated the biofilm biomass. This stimulation of the resistant prey phenotype was not predicted by the model and it was not observed for the biofilm feeders, suggesting the existence of additional mechanisms that stimulate biofilm formation besides selective feeding. Overall, our results confirm our hypothesis that grazing resistance is a matter of the grazers’ trait (i.e. feeding type) rather than a biofilm-specific property.