Wheat PR-1 proteins are targeted by necrotrophic pathogen effector proteins.
Recent studies have identified that proteinaceous effectors secreted by Parastagonospora nodorum are required to cause disease on wheat. These effectors interact in a gene-for-gene manner with host-dominant susceptibilty loci, resulting in disease. However, whilst the requirement of these effectors for infection is clear, their mechanisms of action remain poorly understood. A yeast-two-hybrid library approach was used to search for wheat proteins that interacted with the necrotrophic effector SnTox3. Using this strategy we indentified an interaction between SnTox3 and the wheat pathogenicity-related protein TaPR-1-1, and confirmed it by in-planta co-immunprecipitation. PR-1 proteins represent a large family (23 in wheat) of proteins that are upregulated early in the defence response; however, their function remains ellusive. Interestingly, the P. nodorum effector SnToxA has recently been shown to interact specifically with TaPR-1-5. Our analysis of the SnTox3-TaPR-1 interaction demonstrated that SnTox3 can interact with a broader range of TaPR-1 proteins. Based on these data we utilised homology modeling to predict, and validate, regions on TaPR-1 proteins that are likely to be involved in the SnTox3 interaction. Precipitating from this work, we identified that a PR-1-derived defence signalling peptide from the C-terminus of TaPR-1-1, known as CAPE1, enhanced the infection of wheat by P. nodorum in an SnTox3-dependent manner, but played no role in ToxA-mediated disease. Collectively, our data suggest that P. nodorum has evolved unique effectors that target a common host-protein involved in host defence, albeit with different mechanisms and potentially outcomes.
Plant Sciences Division, Research School of Biology, The Australian National University, Canberra, 2601, Australia.
Susan
S
Breen
School of Chemistry and Molecular Biosciences, Institute for Molecular Bioscience and Australian Infectious Diseases Research Centre, University of Queensland, Brisbane, Australia.
Simon J
SJ
Williams
Plant Sciences Division, Research School of Biology, The Australian National University, Canberra, 2601, Australia.
Britta
B
Winterberg
School of Chemistry and Molecular Biosciences, Institute for Molecular Bioscience and Australian Infectious Diseases Research Centre, University of Queensland, Brisbane, Australia.
Bostjan
B
Kobe
Plant Sciences Division, Research School of Biology, The Australian National University, Canberra, 2601, Australia. peter.solomon@anu.edu.au.
Peter S
PS
Solomon
D001203:Ascomycota / Q000378:metabolism* / Q000472:pathogenicity*; D005656:Fungal Proteins / Q000235:genetics / Q000378:metabolism*; D054884:Host-Pathogen Interactions / Q000235:genetics / Q000502:physiology; D010935:Plant Diseases / Q000235:genetics / Q000382:microbiology*; D010940:Plant Proteins / Q000235:genetics / Q000378:metabolism*; D040641:Quantitative Trait Loci / Q000235:genetics; D014908:Triticum / Q000235:genetics / Q000378:metabolism* / Q000382:microbiology*
D005656:Fungal Proteins; D010940:Plant Proteins

Parastagonospora nodorum
; PR-1; effector triggered susceptibility; effectors; necrotrophic pathogens; wheat