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ARS Home » Plains Area » Fargo, North Dakota » Edward T. Schafer Agricultural Research Center » Cereal Crops Research » Research » Publications at this Location » Publication #274860
Title: A functional genomics approach to dissect the mode of action of the Stagonospora nodorum effector protein SnToxA in wheat

Author
item VINCENT, DELPHINE - Australian National University
item DUFALL, LAUREN - Australian National University
item LIVK, ANDREJA - Proteomics International
item MATHESIUS, ULRIKE - Australian National University
item LIPSCOMBE, RICHARD - Proteomics International
item OLIVER, RICHARD - Curtin University
item Friesen, Timothy
item SOLOMON, PETER - Australian National University

Submitted to: Molecular Plant Pathology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 10/5/2011
Publication Date: 11/24/2011
Citation: Vincent, D., Du Fall, L.A., Livk, A., Mathesius, U., Lipscombe, R.J., Oliver, R.P., Friesen, T.L., Solomon, P.S. 2012. A functional genomics approach to dissect the mode of action of the Stagonospora nodorum effector protein SnToxA in wheat. Molecular Plant Pathology. 13:467-482.

Interpretive Summary: The wheat pathogen Stagonospora nodorum causes disease on wheat by producing pathogen effector proteins that interact with corresponding wheat genes. One such effector, SnToxA, interacts with the Tsn1 gene to contribute towards disease through an unknown mechanism. In this study, proteomics and metabolomics were used to study the host response to SnToxA exposure during a seventy-two hour time course with the aim of understanding how SnToxA contributes to disease. Proteins associated with photosynthesis were observed to marginally increase initially after exposure before decreasing rapidly and significantly. Additionally, several pathways involved in defense response were also differentially regulated including genes involved in an oxidative burst, as well as the increase in abundance of nearly all the known PR proteins, even in the absence of the pathogen. This approach provides further support to the hypothesis that necrotrophic pathogens such as Stagonospora nodorum appear to exploit existing host cell death mechanisms to promote pathogen growth and cause disease.

Technical Abstract: It has now been established that the wheat pathogen Stagonospora nodorum causes disease on wheat in an inverse gene-for-gene manner through the interaction of pathogen effector proteins and corresponding dominant susceptibility host genes. One such effector, SnToxA, interacts with the Tsn1 gene to contribute towards disease through an unknown mechanism. In this study, proteomics and metabolomics were used to study the host response to SnToxA exposure during a seventy-two hour time course with the aim of understanding how SnToxA contributes to disease. Ninety-one unique acidic and basic proteins and 101 metabolites were identified as being significantly different in abundance when comparing SnToxA and control treated wheat leaves during the time course. Proteins associated with photosynthesis were observed to marginally increase initially after exposure before decreasing rapidly and significantly. Proteins and metabolites associated with reactive oxygen species detoxification in the chloroplast were also differentially abundant during SnToxA exposure implying that the disruption of photosynthesis in the chloroplast by the effector causes the rapid accumulation of chloroplastic ROS. Metabolite profiling in the infiltrated leaves revealed major metabolic perturbations in central carbon metabolism evidenced by significant increases in TCA cycle intermediates suggestive of an attempt by the plant to produce energy in response to the collapse of photosynthesis caused by SnToxA. This is supported by the observation that the TCA cycle enzyme malate dehydrogenase was up regulated in response to SnToxA. The infiltration of SnToxA into SnToxA sensitive wheat leaves also resulted in the significant increase in abundance of nearly all the known PR proteins, even in the absence of the pathogen or other pathogen-associated molecular patterns. This approach has highlighted the complementary nature of proteomics and metabolomics in studying effector-host interactions and provides further support to the hypothesis that necrotrophic pathogens such as Stagonospora nodorum appear to exploit existing host cell death mechanisms to promote pathogen growth and cause disease.