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The causal agent of the soybean sudden death syndrome (SDS), Fusarium virguliforme, remains in infected roots and secretes toxins to cause foliar SDS. In this study we investigated the xylem sap, roots, and leaves of F. virguliforme-infected and -uninfected soybean seedlings for any changes in a set of over 3,000 metabolites following pathogen infection by conducting GC/MS and LC/MS/MS, and detected 273 biochemicals. Levels of many intermediates of the TCA cycle were reduced suggesting suppression of this metabolic pathway by the pathogen. There was an increased accumulation of peroxidated lipids in leaves of F. virguliforme-infected plants suggesting possible involvement of free radicals and lipoxygenases in foliar SDS development. Levels of both isoflavone conjugates and isoflavonoid phytoalexins were decreased in infected roots suggesting degradation of these metabolites by the pathogen to promote root necrosis. The levels of the plant immunity inducer pipecolic acid (Pip) and the plant hormone salicylic acid (SA) were significantly increased in xylem sap (in case of Pip) and leaves (in case of both Pip and SA) of F. virguliforme-infected soybean plants compared to the control plants. This suggests a major signaling role of Pip in inducing host defense responses in above ground parts of the F. virguliforme-infected soybean. Increased accumulation of pipecolic acid in foliar tissues was associated with the induction of GmALD1, the soybean homolog of Arabidopsis ALD1. This metabolomics study generated several novel hypotheses for studying the mechanisms of SDS development in soybean., (Copyright © 2015 Elsevier Ireland Ltd. All rights reserved.)

Necrotrophic effectors (also known as host-selective toxins) are important determinants of disease in the wheat-Stagonospora nodorum pathosystem. To date, five necrotrophic effector-host gene interactions have been identified in this system. Most of these interactions have additive effects while some are epistatic. The Snn4-SnTox4 interaction was originally identified in a recombinant-inbred population derived from a cross between the Swiss winter wheat cultivars 'Arina' and 'Forno' using the S. nodorum isolate Sn99CH 1A7a. Here, we used a recombinant-inbred population consisting of 121 lines developed from a cross between the hexaploid land race Salamouni and the hexaploid wheat 'Katepwa' (SK population). The SK population was used for the construction of linkage maps and quantitative trait loci (QTL) detection using the Swiss S. nodorum isolate Sn99CH 1A7a. The linkage maps developed in the SK population spanned 3,228 centimorgans (cM) and consisted of 441 simple-sequence repeats, 9 restriction fragment length polymorphisms, 29 expressed sequence tag sequence-tagged site markers, and 5 phenotypic markers. The average marker density was 6.7 cM/marker. Two QTL, designated QSnb.fcu-1A and QSnb.fcu-7A on chromosome arms 1AS and 7AS, respectively, were associated with disease caused by the S. nodorum isolate Sn99CH 1A7a. The effects of QSnb.fcu-1A were determined by the Snn4-SnTox4 interaction and accounted for 23.5% of the phenotypic variation in this population, whereas QSnb.fcu-7A accounted for 16.4% of the phenotypic variation for disease but was not associated with any known effector sensitivity locus. The effects of both QTL were largely additive and collectively accounted for 35.7% of the total phenotypic variation. The results of this research validate the effects of a compatible Snn4-SnTox4 interaction in a different genetic background, and it provides knowledge regarding genomic regions and molecular markers that can be used to improve Stagonospora nodorum blotch resistance in wheat germplasm.