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Phytophthora sojae causes Phytophthora root and stem rot of soybean and has been primarily managed through deployment of qualitative Resistance to P. sojae genes (Rps genes). The effectiveness of each individual or combination of Rps gene(s) depends on the diversity and pathotypes of the P. sojae populations present. Due to the complex nature of P. sojae populations, identification of more novel Rps genes is needed. In this study, phenotypic data from previous studies of 16 panels of plant introductions (PIs) were analyzed. Panels 1 and 2 consisted of 448 Glycine max and 520 G. soja, which had been evaluated for Rps gene response with a combination of P. sojae isolates. Panels 3 and 4 consisted of 429 and 460 G. max PIs, respectively, which had been evaluated using individual P. sojae isolates with complex virulence pathotypes. Finally, Panels 5-16 (376 G. max PIs) consisted of data deposited in the USDA Soybean Germplasm Collection from evaluations with 12 races of P. sojae. Using these panels, genome-wide association (GWA) analyses were carried out by combining phenotypic and SoySNP50K genotypic data. GWA models identified two, two, six, and seven novel Rps loci with Panels 1, 2, 3, and 4, respectively. A total of 58 novel Rps loci were identified using Panels 5-16. Genetic and phenotypic dissection of these loci may lead to the characterization of novel Rps genes that can be effectively deployed in new soybean cultivars against diverse P. sojae populations., (© 2020 The Authors. The Plant Genome published by Wiley Periodicals LLC on behalf of Crop Science Society of America.)

Key Message: Novel QTL conferring resistance to both the SDS and SCN was detected in two RIL populations. Dual resistant RILs could be used in breeding programs for developing resistant soybean cultivars. Soybean cultivars, susceptible to the fungus Fusarium virguliforme, which causes sudden death syndrome (SDS), and to the soybean cyst nematode (SCN) (Heterodera glycines), suffer yield losses valued over a billion dollars annually. Both pathogens may occur in the same production fields. Planting of cultivars genetically resistant to both pathogens is considered one of the most effective means to control the two pathogens. The objective of the study was to map quantitative trait loci (QTL) underlying SDS and SCN resistances. Two recombinant inbred line (RIL) populations were developed by crossing 'A95-684043', a high-yielding maturity group (MG) II line resistant to SCN, with 'LS94-3207' and 'LS98-0582' of MG IV, resistant to both F. virguliforme and SCN. Two hundred F 7 derived recombinant inbred lines from each population AX19286 (A95-684043 × LS94-3207) and AX19287 (A95-684043 × LS98-0582) were screened for resistance to each pathogen under greenhouse conditions. Five hundred and eighty and 371 SNP markers were used for mapping resistance QTL in each population. In AX19286, one novel SCN resistance QTL was mapped to chromosome 8. In AX19287, one novel SDS resistance QTL was mapped to chromosome 17 and one novel SCN resistance QTL was mapped to chromosome 11. Previously identified additional SDS and SCN resistance QTL were also detected in the study. Lines possessing superior resistance to both pathogens were also identified and could be used as germplasm sources for breeding SDS- and SCN-resistant soybean cultivars.

Phytophthora sojae Kaufmann and Gerdemann, which causes Phytophthora root rot, is a widespread pathogen that limits soybean production worldwide. Development of Phytophthora resistant cultivars carrying Phytophthora resistance Rps genes is a cost-effective approach in controlling this disease. For this mapping study of a novel Rps gene, 290 recombinant inbred lines (RILs) (F7 families) were developed by crossing the P. sojae resistant cultivar PI399036 with the P. sojae susceptible AR2 line, and were phenotyped for responses to a mixture of three P. sojae isolates that overcome most of the known Rps genes. Of these 290 RILs, 130 were homozygous resistant, 12 heterzygous and segregating for Phytophthora resistance, and 148 were recessive homozygous and susceptible. From this population, 59 RILs homozygous for Phytophthora sojae resistance and 61 susceptible to a mixture of P. sojae isolates R17 and Val12-11 or P7074 that overcome resistance encoded by known Rps genes mapped to Chromosome 18 were selected for mapping novel Rps gene. A single gene accounted for the 1:1 segregation of resistance and susceptibility among the RILs. The gene encoding the Phytophthora resistance mapped to a 5.8 cM interval between the SSR markers BARCSOYSSR_18_1840 and Sat_064 located in the lower arm of Chromosome 18. The gene is mapped 2.2 cM proximal to the NBSRps4/6-like sequence that was reported to co-segregate with the Phytophthora resistance genes Rps4 and Rps6. The gene is mapped to a highly recombinogenic, gene-rich genomic region carrying several nucleotide binding site-leucine rich repeat (NBS-LRR)-like genes. We named this novel gene as Rps12, which is expected to be an invaluable resource in breeding soybeans for Phytophthora resistance., Competing Interests: The authors have declared that no competing interests exist.

Soybean cultivars with specific single resistance genes (Rps) are grown to reduce yield loss due to Phytophthora stem and root rot caused by the oomycete pathogen Phytophthora sojae. To identify novel Rps loci, soybean lines are often screened several times, each time with an isolate of P. sojae that differs in virulence on various Rps genes. The goal of this study was to determine whether several isolates of P. sojae that differ in virulence on Rps genes could be combined into a single source of inoculum and used to screen soybean lines for novel Rps genes. A set of 14 soybean differential lines, each carrying a specific Rps gene, was inoculated with three isolates of P. sojae, which differed in virulence on 6 to 10 Rps genes, individually or in a 1:1:1 mixture. Inoculum containing the 1:1:1 mixture of isolates was virulent on 13 Rps genes. The mixed-inoculum method was used to screen 1,019 soybean accessions in a blind assay for novel sources of resistance. In all, 17% of Glycine max accessions and 11% of G. soja accessions were resistant (≤30% dead plants), suggesting that these accessions may carry a novel Rps gene or genes. Advantages of combining isolates into a single source of inoculum include reduced cost, ability to screen soybean germplasm with inoculum virulent on all known Rps genes, and ease of identifying novel sources of resistance. This study is a precursor to identifying novel sources of resistance to P. sojae in soybean using RXLR effectors.

Key Message: Soybean deploys multiple genetic mechanisms to confer tolerance to Fusarium virguliforme toxins. This study revealed that F. virguliforme culture filtrates could be used in mapping QTL underlying foliar SDS resistance. Sudden death syndrome (SDS) is a major soybean disease throughout most of the soybean growing regions in the world including the United States. The disease is caused by the fungal pathogen, Fusarium virguliforme (Fv). The fungus produces several toxins that are responsible for development of interveinal leaf chlorosis and necrosis, which are typical foliar SDS symptoms. Growing of resistant cultivars has been the most effective method in controlling the disease. The objective of the present study was to identify quantitative trait loci (QTL) underlying host responses of soybean to Fv toxins present in culture filtrates. To accomplish this objective, two recombinant inbred line (RIL) populations, AX19286 (A95-684043 × LS94-3207) and AX19287 (A95-684043 × LS98-0582), segregating for SDS resistance were evaluated for foliar symptom development by applying two screening protocols, the stem cutting and the root feeding assays. The AX19286 population revealed two major and seven minor QTL for SDS resistance. In the AX19287 population, we identified five major QTL and three minor QTL. The two QTL mapped to Chromosome 7 [molecular linkage group (MLG) M] and Chromosome 20 (MLG I) are most likely novel, and were detected through screening of the AX19287 population with stem cutting and root feeding assays, respectively. This study established that Fv culture filtrates could be employed in mapping QTL underlying foliar SDS resistance. The outcomes of the research also suggest that multiple genetic mechanisms might be used by soybean to overcome the toxic effects of the toxins secreted by the pathogen into culture filtrates.

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.)

Background: Sudden death syndrome (SDS) caused by the ascomycete fungus, Fusarium virguliforme, exhibits root necrosis and leaf scorch or foliar SDS. The pathogen has never been identified from the above ground diseased foliar tissues. Foliar SDS is believed to be caused by host selective toxins, including FvTox1, secreted by the fungus. This study investigated if the xylem sap of F. virguliforme-infected soybean plants contains secreted F. virguliforme-proteins, some of which could cause foliar SDS development., Results: Xylem sap samples were collected from five biological replications of F. virguliforme-infected and uninfected soybean plants under controlled conditions. We identified five F. virguliforme proteins from the xylem sap of the F. virguliforme-infected soybean plants by conducting LC-ESI-MS/MS analysis. These five proteins were also present in the excreted proteome of the pathogen in culture filtrates. One of these proteins showed high sequence identity to cerato-platanin, a phytotoxin produced by Ceratocystis fimbriata f. sp. platani to cause canker stain disease in the plane tree. Of over 500 soybean proteins identified in this study, 112 were present in at least 80% of the sap samples collected from F. virguliforme-infected and -uninfected control plants. We have identified four soybean defense proteins from the xylem sap of F. virguliforme-infected soybean plants. The data have been deposited to the ProteomeXchange with identifier PXD000873., Conclusion: This study confirms that a few F. virguliforme proteins travel through the xylem, some of which could be involved in foliar SDS development. We have identified five candidate proteinaceous toxins, one of which showed high similarity to a previously characterized phytotoxin. We have also shown the presence of four soybean defense proteins in the xylem sap of F. virguliforme-infected soybean plants. This study laid the foundation for studying the molecular basis of foliar SDS development in soybean and possible defense mechanisms that may be involved in conferring immunity against F. virguliforme and other soybean pathogens.

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.

Stagonospora nodorum, casual agent of Stagonospora nodorum blotch (SNB) of wheat, produces a number of host-selective toxins (HSTs) known to be important in disease. To date, four HSTs and corresponding host sensitivity genes have been reported, and all four host-toxin interactions are significant factors in the development of disease. Here, we describe the identification and partial characterization of a fifth S. nodorum produced HST designated SnTox4. The toxin, estimated to be 10-30 kDa in size, was found to be proteinaceous in nature. Sensitivity to SnTox4 is governed by a single dominant gene, designated Snn4, which mapped to the short arm of wheat chromosome 1A in a recombinant inbred (RI) population. The compatible Snn4-SnTox4 interaction is light dependent and results in a mottled necrotic reaction, which is different from the severe necrosis that results from other host-toxin interactions in the wheat-S. nodorum pathosystem. QTL analysis in a population of 200 RI lines derived from the Swiss winter wheat varieties Arina and Forno revealed a major QTL for SNB susceptibility that coincided with the Snn4 locus. This QTL, designated QSnb.fcu-1A, explained 41.0% of the variation in disease on leaves of seedlings indicating that a compatible Snn4-SnTox4 interaction plays a major role in the development of SNB in this population. Additional minor QTL detected on the short arms of chromosomes 2A and 3A accounted for 5.4 and 6.0% of the variation, respectively. The effects of the three QTL were largely additive, and together they explained 50% of the total phenotypic variation. These results provide further evidence that host-toxin interactions in the wheat-S. nodorum pathosystem follow an inverse gene-for-gene model.