callum.verdonk@curtin.edu.au

kar-chun.tan@curtin.edu.au

Septoria nodorum blotch (SNB) is a devastating disease of wheat and is caused by the fungal pathogen Parastagonospora nodorum. The primary cause of SNB is proteinaceous effectors, which interact with wheat host sensitivity genes.

These effectors are controlled by DNA-binding regulatory proteins called transcription factors (TF), of which the Zn2Cys6 zinc-finger type is one of the most abundant in fungi. These zinc-finger-containing TFs possess a DNA-binding domain (DBD) and central “middle homology domain” (MHD). In P. nodorum the TF PnPf2 is a positive regulator of major necrotrophic effector genes required for host-specific virulence on wheat.

PnPf2 is a DBD-MHD protein with a disordered C-terminus tail which has low homology with its orthologs. We demonstrated that the DBD and MHD are essential for PnPf2 function but are not the main drivers of pathogenicity. Instead, only the disordered C-terminus tail is seemingly required for both effector activation, as well as disease symptoms on wheat.

These observations indicate a novel, uninvestigated mode of action by zinc-finger TFs, not currently characterised in other fungal pathogens. By understanding the structural and biological mechanisms of PnPf2, we can develop novel strategies to minimise the impact of effector-mediated diseases like SNB across Australia and worldwide.