The Phytochemical Landscape and Pathogen Evolutionary Ecology

The Phytochemical landscape of plants offers a powerful tool to examine the evolutionary arms race between hosts and pathogens. Leaves and stems are fortified with a chemically diverse arsenal of metabolites, including phenolics, terpenes, and alkaloids, many of which act as antimicrobial compounds. Yet pathogens like Botrytis cinerea (a generalist necrotrophic fungus infecting hundreds of host species across the plant kingdom) demonstrate remarkable success in colonizing despite these barriers. This paradox suggests that B. cinerea employs an array of strategies to navigate, neutralize, or even co-opt plant chemical defenses.

This raises a central question: How does a generalist pathogen survive and thrive in such chemically heterogeneous environments? Does it rely on broad-spectrum detoxification pathways, flexible gene networks, or finely tuned mechanisms specific to different chemical classes?

To address these questions, my group leverages genome-wide association and population-level analyses to connect natural genetic variation in B. cinerea with phenotypic responses to specialized metabolites. Rather than focusing on a single isolate, this framework allows us to ask:

•	Which detoxification enzymes and transporters are most critical for resistance?

•	Is resistance polygenic, spread across numerous loci of small effect, or concentrated in a handful of major pathways?

•	How do these genetic strategies map onto ecological interactions with chemically diverse hosts?

By integrating chemical ecology, quantitative genetics, and fungal toxicology, we aim to move beyond static host–pathogen models. Our goal is to build a population-level view of resistance, one that captures both the breadth of B. cinerea’s generalism and the fine-scale mechanisms that enable survival in chemically defended environments. This approach not only illuminates the evolutionary ecology of a globally important pathogen, but also offers opportunities for collaboration across plant biology, genomics, and metabolomics to redefine how we study host–pathogen interactions.