Identification of host targets of Fusarium effector proteins provides insight in disease resistance and susceptibility.
Vascular wilt diseases are a major problem in agriculture, Fusarium oxysporum being an infamous example infecting over 100 important crop species. To develop new strategies to combat pathogens a better understanding of the molecular mechanisms underlying disease and resistance are essential. To reveal the host processes targeted by this fungus we use the secreted effector proteins as probes to identify their host targets. These targets are candidate susceptibility (S) genes, and their mutation is expected to interfere with the ability of the fungus to manipulate the host. As some of these targets are guarded by resistance (R) genes our studies also provide insight in strategies used by the pathogen to overcome resistance while retaining virulence. In this presentation I will focus on two effectors; a) the Avr2/Six5 effector pair targeting plasmodesmata facilitating their cell-to-cell movement allowing Avr2 to compromise PAMP triggered immunity by targeting Bik1 and b) Six8 which was found to target specific members of the topless (TPL) family, transcriptional regulators involved in a plethora of signaling processes. We could show that TPLs can function as S genes for Fusarium wilt. Furthermore, we found that in Arabidopsis TPLs are guarded by the R protein SNC1.