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functional genomics approach to dissect the mode of action of the Stagonospora nodorum effector protein SnToxA in wheat.

Vincent, Delphine, Du Fall, Lauren A., Livk, Andreja, Mathesius, Ulrike, Lipscombe, Richard J., Oliver, Richard P., Friesen, Timothy L., Solomon, Peter S.
Molecular plant pathology 2012 v.13 no.5 pp. 467
Leptosphaeria nodorum, carbon, cell death, chloroplasts, energy, fungal proteins, gene-for-gene relationship, genes, genomics, host-pathogen relationships, leaves, malate dehydrogenase, mechanism of action, metabolites, metabolomics, mycotoxins, pathogenesis, photosynthesis, plant pathogenic fungi, proteomics, reactive oxygen species, tricarboxylic acid cycle, wheat
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.