Identification of septoria nodorum blotch responsive QTLs in wheat through the removal of defined necrotrophic effector-host sensitivity gene interactions 
H. PHAN (1), K. Rybak (1), E. Furuki (1), R. Oliver (1) (1) Curtin University, Australia

The fungus Parastagonospora nodorum is a causal agent of septoria nodorum blotch (SNB) on wheat. P. nodorum causes significant yield reduction of wheat despite the application of fungicides and a heavy focus over the last 30 years on traditional breeding for resistance. The discovery of necrotrophic effectors has given breeding for disease resistance new methods and tools. Three effector-host sensitivity gene systems are well characterised in this pathosystem; SnToxA-Tsn1, SnTox1-Snn1 and SnTox3-Snn3. Genetic analysis of various mapping populations and pathogen isolates has shown that different effectors have varying impact and that epistatic interactions also occur. As a result of these factors the deployment of these effectors for SNB resistance breeding is difficult. In this study, we have deleted genes that code for SnToxA, 1 and 3 in P. nodorum (toxa13). Effector activity and disease potential toxa13 were assessed using wheat mapping populations. Disease infection assay showed that toxa13 was able to cause SNB incidence as high as the wild-type, suggesting that other interactions are operating in the system. Interval quantitative trait locus (QTL) mapping has unmasked a significant SNB QTL on 2DS that coincided with location of the Snn2 susceptibility locus. This QTL was not observed in the wild-type. This research also uncovered novel QTLs responding to SNB and effectors sensitivity on 2AS1 and 3AL of wheat chromosomes. Further studies are being carried out to investigate the novel interactions including P. nodorum necrotic effector and receptor/susceptibility QTL identifications. 

Abstract Number: P17-585
Session Type: Poster