Swammerdam Institute for Life Sciences

Research line dr. M. (Martijn) Rep

Fungal pathogenicity

A central question for us is how a fungus is able to colonize a living plant, thereby overcoming the basal resistance responses that plants have evolved against microbial invasion. Even if successful in overcoming basal resistance, fungal colonization can be resisted through a second layer of the plant’s immune system (R proteins) which recognizes specific compounds secreted by the fungus. Ironically, these compounds are usually small proteins, called effectors, that the fungus secretes to suppress immunity or otherwise promote host colonization. Thus, plant and fungus are locked in a molecular arms race involving relatively fast-evolving pathogen effectors and their matching immune receptors in the host

We use the interaction between the vascular pathogen Fusarium oxysporum and host plants (primarily tomato) to study these molecular interactions and their evolution. Using xylem sap proteomics, we have now identified all three tomato R protein-recognized effectors (Avr's) of F. oxysporum f.sp. lycoperscici (Fol) as small, in planta-secreted proteins. Remarkably, Avr1 suppresses the R protein-mediated resistance that is normally triggered by Avr2 and Avr3, exposing a complicated interaction between Avr's and R proteins. We have also identified additional in planta-secreted proteins including potential effectors. Through gene knockout, we have shown that several of these also contribute to virulence

The genes for effectors of F. oxysporum reside on lineage-specific, supernumerary chromosomes at least some of which can be transferred horizontally between otherwise genetically isolated clonal lines. We have recently embarked on a project to uncover the mechanism of this process and to infer its evolutionary consequences, including the emergence of host-specific pathogenicity within the F. oxysporum species complex

10 December 2012