2018 ESA Annual Meeting (August 5 -- 10)

COS 138-7 - Understanding plant defense syndromes: Using dynamical models to explain multivariate plant defenses

Friday, August 10, 2018: 10:10 AM
239, New Orleans Ernest N. Morial Convention Center
Collin B. Edwards, Department of Biology, Tufts University, Medford, MA and Stephen Ellner, Department of Ecology and Evolutionary Biology, Cornell University, Ithaca, NY
Background/Question/Methods

Empirical studies have found that plants tend to invest in sets of defense traits that together form syndromes; there is some evidence that these syndromes tradeoff with one another, but empirical studies have shown conflicting results. Numerous theories exist to explain when and where plants should be more or less defended against herbivores, but the field lacks a framework for predicting which traits should fall into the same syndromes, and when one defense syndrome should be favored over another. Here we use a simple dynamical model of herbivore and plant growth to explore the consequences of plants investing defense resources in one or more trait(s). Rather than deal with specific defense traits, we focus on “defense modes”, defined by the mechanisms that impact herbivores. Our model includes defense modes that increase handling time (e.g. trichomes), decrease conversion efficiency (e.g. protease inhibitors), or kill herbivores outright (toxins). We use our model to explore which combinations of defense modes form beneficial syndromes, and how other life history traits determine which syndrome is favored.

Results/Conclusions

We found several favorable defense syndromes, but which syndrome was optimal depended on the level of plant investment in defense and on the plant intrinsic growth rate. When the plant invested little in defense, it benefited most by investing only in toxins. For intermediate defense investment, the optimal syndrome was a combination of increased handling time and decreased conversion efficiency. For very high levels of defense investment, the optimal syndrome was solely handling time defenses. While there was a small window of defense investment when the optimal strategy was equal investment in all three defense modes, our model predicts plants generally falling into defense syndromes of (a) toxins or (b) handling time and conversion efficiency defenses, or (c) just handling time defenses, depending on defense investment. Variation in intrinsic growth rate showed qualitatively the same pattern: plants with low growth rates should have syndrome (a), plants with intermediate growth rates should have syndrome (b), and plants with high growth rates should have syndrome (c). Our model provides a theoretical framework for understanding and predicting defense syndromes, and can help us interpret the conflicting defense syndrome empirical literature.