The Fusarium oxysporum effector pair Avr2 & Six5 in action

Plants are continuously challenged by pathogenic microbes lurking in the environment. Successful pathogens can overcome plant defences and colonize host plants and manipulate them to provide nutrients and shelter. To combat adapted pathogens resistant hosts have developed the ability to detect specific effector proteins via resistance (R) genes. Six3 and Six5 are effectors from Fusarium oxysporum f.sp. lycopersici (Fol). Fol is the causal agent of vascular wilt disease in tomato. The SIX3 - SIX5 effector pair shares their promoter region and deletion of either SIX3 or SIX5 compromises fungal pathogenicity. Besides being virulence factors, Six3 and Six5 are both required to trigger the tomato I-2 R protein-mediated resistance in tomato following Fol infection. Avr2 and Six5 can physically interact in planta. Moreover, Avr2 and Six5 specifically interact at plasmodesmata in subsequent bimolecular fluorescence complementation assays. Single-cell transformation assays showed that Avr2 and Six5 together seem to function as a fungal movement protein by altering plasmodesmatal transductivity expanding their exclusion limit for symplastic protein transport. Both Avr2 and Six5 have the ability to suppress flg22-induced immune responses. However, only Avr2 altered Arabidopsis susceptibility to various bacterial and fungal pathogens (Pseudomonas syringae, Verticillium dahliae and Fusarium oxysporum). These data suggest that Avr2 functions as a virulence factor by targeting PAMP triggered immune signalling, while the main role of Six5 in Fol pathogenicity lies in facilitating Avr2 function. A working model is provided detailing how the Avr2/Six5 effector pair might confer virulence and I-2-mediated avirulence following Fol colonization of tomato roots.