EVOLUTIONARY ECOLOGY OF PLANT DISEASE

Together with collaborator Greg Gilbert, I study the population-level impacts of plant pathogens in natural systems, including the mechanistic drivers that link disease pressure to ecological conditions (e.g., Bradley et al. 2003).  This exciting field brings together evolutionary and ecological dynamics, cutting edge molecular approaches, and phylogenetic ecology.

NOVEL HOST-PATHOGEN INTERACTIONS

droppedImage-1Also see “Testing the natural enemies hypothesis,” below.
In a set of review papers, Greg and I have explored the evolutionary ecology of novel plant-pathogen interactions, including applications to emerging epidemics, invasive plants, biological control with plant pathogens, and agriculture and forestry (Parker and Gilbert 2004, Gilbert and Parker 2006).  We also participated in an NCEAS working group run by Charles Mitchell and Sunny Power, which explored some of these same themes (Mitchell et al. 2006).

porrocaPorrocaLogoPorroca is a novel disease of coconut palm that is spreading rapidly from Colombia through Panama, with potentially devastating impacts on the economy of the Kuna Indians, the principal indigenous community of the Caribbean coast of the isthmusUltimately, this project is aimed at helping to solve a potentially devastating socioeconomic problem for the Kuna. Additionally, the project will contribute toward models for the spread of invasive new diseases across landscapes. Collaborative work with Nigel Harrison points to a Stolbur-group phytoplasma as the cause of the disease, and we are working to elucidate the basic biology of the disease and seek control options (Gilbert and Parker 2008). 

RARE SPECIES ADVANTAGE: CONSEQUENCES OF NUMERICAL AND PHYLOGENETIC RARITY FOR DISEASE PRESSURE AND PATHOGEN COMMUNITIES

shapeimage_2Locally rare species are expected to have a survival advantage over more abundant species, because rarity reduces their risk of damage from pathogens. This “rare-species advantage” may help maintain plant diversity in natural systems and explain how introduced plant species become invasive weeds. However, most pathogens are able to infect a variety of different hosts. Which hosts are susceptible is not a random assortment of species, because closely related species are more likely to share a pathogen than are more distantly related species. This means that rarity is not simply a function of species density (numerical rarity), but of the combined density of all species with which it shares a pathogen. A species with no closely related neighbors has the added benefit of “phylogenetic rarity”.

Postdoc Megan Saunders, Greg Gilbert, and I are evaluating the relative importance of phylogeny and abundance in the rare-species advantage in several plant communities along the Central Coast of California.  In addition, in a sentinel plant experiment we directly test how phylogenetic rarity influences the tendency of an introduced plant to “escape disease.”  Finally, we are using 454 sequencing approaches to characterize how foliar fungal communities are structured across host species, testing critical assumptions about pathogen-sharing.

TESTING THE NATURAL ENEMIES HYPOTHESIS OF INVASION: NATIVE, INTRODUCED, AND INVASIVE CLOVERS

impA common assertion is that invasions occur because species “leave their natural enemies behind” and are therefore released from pest pressure to become aggressive competitors in their introduced range.  Greg Gilbert and I tested the Natural Enemies Hypothesis by comparing herbivory as well as pathogen diversity, infection rates, symptoms, and fitness effects on a suite of 18 native and introduced clover species, adding a novel comparison of introduced species that invade vs. those that don’t.  We found little evidence for the idea that The Natural Enemies Hypothesis can explain invasiveness in this system, or indeed, that any sort of escape from pathogens has occurred (Parker and Gilbert 2007).

droppedImage_3One possible explanation for a lack of ecological “escape from pathogens” is that rapid evolution in the pathogens quickly increases infection of and virulence on the new hosts, equalizing pest pressure (Parker and Gilbert 2004, Gilbert and Parker 2006).  In order to explore the evolutionary processes behind novel host-pathogen dynamics, we created “de novo introductions”, with serial passage experiments on California pathogens with clover hosts collected from Europe and parallel experiments with native and introduced clover hosts collected from California. We found intriguing evidence for rapid evolution in infectivity over five generations in the greenhouse, and in virulence over historical time (Gilbert and Parker 2010).

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