The fungus Parastagonospora nodorum causes septoria nodorum blotch (SNB) of wheat by secreting a suite of proteinaceous necrotrophic effectors (NEs) to induce tissue necrosis upon infection. Tox effectors only induce necrosis/chlorosis on wheat cultivars that possess matching dominant susceptibility genes (Snn).

It has been demonstrated that multiple NE-Snn interactions dictate the outcome of SNB through additive but also epistatic interactions. In this study, we have generated a P. nodorum mutant (toxa13) that lacked major NE genes; SnToxA, SnTox1 and SnTox3. Surprisingly, the virulence of P. nodorum toxa13 is comparable to the wildtype on modern bread wheats despite ablating three NE-Snn interactions.

This suggests that other functionally redundant pathogenicity mechanisms compensate for the loss of the three major effectors. A comparative RNA-Seq study revealed that the NE gene SnTox267 and two phytotoxic secondary metabolite (SM) gene clusters were highly up-regulated in toxa13 in-planta.

Furthermore, several candidate NE genes, uncharacterised SM gene clusters and signal transduction genes were also found to be up-regulated and may contribute to maintaining the virulence of toxa13. Characterisation of these genes for their role in the sustained virulence of P. nodorum toxa13 will be discussed.