Research line dr. ing. F.L.W. (Frank) Takken
Plant disease resistance
In this research line, we aim to uncover the molecular mechanisms of gene-for-gene based resistance in plants and strategies employed by pathogens to overcome disease resistance. Resistance (R) proteins recognize specific pathogens and subsequently trigger the activation of defense responses that restrict pathogen ingress. Three major research questions are: (i) How do R proteins function? (ii) How is defense signaling activated and what is the role of post-translational modifications in this process? And (iii) how does a pathogen avoid or suppress defense responses?
The main model is the interaction between tomato and the soil-borne fungal pathogen Fusarium oxysporum fsp. lycopersici (Fol). During infection the fungus secretes many small proteins (effectors) in the xylem sap of the host. Some of these effectors are unintentionally recognized by a plant R protein, resulting in activation of host defenses. One example is the effector protein Avr2 that is recognized by the tomato I-2 resistance protein. Most R proteins, including I-2, belong to the large family of NBS-LRR proteins. These proteins contain a central nucleotide-binding (NB) domain, an N-terminal coiled-coil domain and a C-terminal Leucine Rich Repeat (LRR) domain. To understand how R proteins function we study their nucleotide binding properties and their intramolecular interactions. To understand how R proteins activate defenses we use them as baits to identify interacting partners. From the pathogen side we investigate the ability of Fol effectors to interfere with host defense inductio
Plant defenses are normally suppressed in the absence of a pathogen and the Small Ubiquitin-like MOdifier (SUMO) protein seems to play a role in this process. Recently we discovered that SUMO affects salicylic acid-dependent gene expression and acts as a transcriptional repressor. We are currently investigating how this gene repression is released upon pathogen attack and allows activation of the defense response upon infection