Location: Cereal Crops ResearchTitle: A necrotrophic effector from Parastagonospora nodorum triggers programmed cell death by targeting two distinct non-homoeologous wheat sensitivity genes
|RICHARDS, JONATHAN - North Dakota State University
|KARIYAWASAM, GAYAN - North Dakota State University
|LIU, ZHAOHUI - North Dakota State University
Submitted to: International Congress on Molecular Plant-Microbe Interactions
Publication Type: Abstract Only
Publication Acceptance Date: 7/14/2019
Publication Date: N/A
Interpretive Summary: .
Technical Abstract: Parastagonospora nodorum, a necrotrophic fungal pathogen of wheat, uses an array of necrotrophic effector (NE) proteins to facilitate disease. The perception of NEs by host sensitivity proteins results in the initiation of programmed cell death (PCD). Nine NE-sensitivity gene interactions have been observed within this pathosystem, however, genes encoding SnTox2 or SnTox6 remain undiscovered. Genome sequencing of 198 P. nodorum isolates and phenotyping of host differential lines enabled an association mapping (AM) approach to identify novel NEs. AM using 322,613 polymorphisms identified a locus associated with virulence on differential lines BG223 (Snn2) and ITMI37 (Snn6) and harbored a candidate gene encoding a predicted effector. Disruption of SnTox2/6 in isolate Sn4 resulted in the loss of virulence on both Snn2+ and Snn6+ lines, as well as failure to detect Snn2 and Snn6 QTL when inoculated onto the BG and ITMI populations, respectively. Transformation of avirulent isolate Sn79-1087 with SnTox2/6 resulted in virulence on lines harboring Snn2 or Snn6, as well as detection of the aforementioned QTL. SnTox2/6 is upregulated in planta, reaching peak expression at 24 hr post-inoculation. Putative epistatic interactions were also detected, with the deletion of SnTox2/6 affecting the efficacy of SnTox1 or SnTox3 interactions with corresponding sensitivity genes. The results indicate SnTox2/6 is a single NE which elicits PCD via detection by two non-homoeologous host targets.