Research

Origins of plant disease outbreaks

We run collaborative field programs to uncover the origins of infectious disease outbreaks in crop plants. Sequence-informed sampling across regions and hosts suspected of harboring disease reservoirs allows us to reconstruct outbreak origins, pathways of pathogen dissemination and the evolutionary processes underlying disease emergence events. We work on outbreaks caused by Pseudomonas spp. and Ralstonia spp. on multiple plants hosts. Some examples of this work are here and here. Check out this video highlighting our Indonesian field program with Universitas Gadjah Mada.

Mobile elements driving adaptation

Horizontal gene transfer and homologous recombination contribute to rapid evolution in bacterial pathogens. Mobile elements such as integratives and conjugative elements (ICEs) introduce antimicrobial resistance and virulence-related genes to bacterial pathogens. We have found mobile elements are rapidly exchanged during disease outbreaks and can have surprising consequences for the bacterial host. We investigate the dynamics of horizontal transfer during outbreak events and use lab experiments to test transfer frequency variation and fitness consequences of variable accessory gene carriage in different host backgrounds.

Intermicrobial antagonism

Bacterial pathogens encounter multiple threats from other microbes during host infection, including phage attack, toxin delivery and competition for scarce nutrient resources. Contact-dependent inhibition (CDI) is a mechanism of self-recognition and interbacterial antagonism mediated by Type 5b secretion systems that allows cells to detect and inhibit the growth on competitors. We study how CDI evolve in plant pathogenic bacteria, how CDI alters host infection outcomes to structure within-host diversity, and its application for targeted pathogen control.

Host-pathogen interactions

Bacterial pathogens deploy Type 3 secretion systems to inject virulence proteins directly into plant cells. Plant hosts in turn have evolved proteins that can detect the activity of pathogen virulence proteins and mount rapid resistance responses. These interactions result in host-pathogen coevolutionary arms races marked by the rapid diversification of pathogen virulence and host resistance genes. We explore how virulence proteins evolve in both wild and agricultural pathogen populations and sequence wild host populations to uncover resistance gene diversity and genes that may be coevolving with endemic pathogen populations. Read more about this here.