Differential effector gene expression underpins epistasis in a plant fungal disease

HTT Phan1, K Rybak1, E Furuki1, S Breen2, PS Solomon2, RP Oliver1 and KC Tan1

  1. Centre for Crop and Disease Management, Department of Environment and Agriculture, Curtin University, Bentley WA 6102, Australia
  2. Plant Sciences Division, Research School of Biology, The Australian National University, Canberra, Australia

Fungal effector-host sensitivity gene interactions play a key role in determining the outcome of septoria nodorum blotch disease (SNB) caused by the fungus Parastagonospora nodorum on wheat. The pathosystem is complex and mediated by interaction of multiple fungal proteinaceous necrotrophic effector-host sensitivity gene systems. Three effector-sensitivity gene systems are well characterised in this pathosystem; SnToxA-Tsn1, SnTox1-Snn1 and SnTox3-Snn3. A wheat mapping population that segregated for Snn1 and Snn3 was infected with an aggressive effector-producing P. nodorum wild-type isolate to study the inheritance of sensitivity to SnTox1 and SnTox3 and disease susceptibility. Interval quantitative trait locus (QTL) mapping demonstrated that the SnTox1-Snn1 interaction was paramount in the development of SNB on both seedlings and adult plants. However, the SnTox3-Snn3 interaction was not observed when infected with the wild-type strain. The SnTox3-Snn3 interaction was only detected in a strain of the wild-type where SnTox1 had been deleted via homologous recombination (tox1-6). Gene expression analysis indicates increased SnTox3 expression in tox1-6 compared to the wild-type. This indicates that the failure to detect the SnTox3-Snn3 interaction in the wild-type is due – at least in part – to suppressed expression of SnTox3 mediated by SnTox1. In addition, infection with a P. nodorum strain carrying SnToxA, SnTox1 and SnTox3 deletions (toxa13) uncovered a significant SNB QTL on the short arm of chromosome 2D where the SnTox2 effector sensitivity gene, Snn2, is located. This QTL was not observed in the wild-type and tox1-6 infections and thus suggesting that SnToxA and/or SnTox3 were epistatic. Additional QTLs responding to SNB and effector sensitivity were detected on chromosomes 2A and 3A.