Kar-Chun.Tan@curtin.edu.au

The fungus Parastagonospora nodorum causes septoria nodorum blotch (SNB) on wheat. The phytopathogen secretes proteinaceous necrotrophic effectors to cause necrosis on wheat carrying a dominant susceptibility phenotype leading to SNB. The coordination of effector and pathogenicity gene expression by signalling pathways is a topic of intense investigation.

In this study, we used a reverse genetic approach to dissect the role of the fungal Velvet-family transcription factor VeA in P. nodorum development and virulence on wheat. P. nodorum mutants carrying VeA (PnVeA) deletion displayed vegetative growth abnormalities, altered pigmentation, lost the ability to produce asexual spores and demonstrated a strong reduction in its ability to infect wheat. Comparative RNA-Seq and RT-PCR analyses revealed that the deletion of PnVeA decoupled the expression of major necrotrophic effector genes.

In addition, the deletion of PnVeA resulted in an up-regulation of four predicted secondary metabolite (SM) gene clusters. Using liquid-chromatography mass-spectrometry, it was observed that an increase in the expression of the alternariol SM gene cluster led to an accumulation of the mycotoxin.

Our study has shown that PnVeA is essential for asexual sporulation, full virulence, secondary metabolism and necrotrophic effector regulation.