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ARS Home » Midwest Area » Urbana, Illinois » Soybean/maize Germplasm, Pathology, and Genetics Research » Research » Publications at this Location » Publication #312011

Research Project: IMPROVED RESISTANCE TO SOYBEAN PATHOGENS AND PESTS

Location: Soybean/maize Germplasm, Pathology, and Genetics Research

Title: Identification of multiple phytotoxins produced by Fusarium virguliforme including a phytotoxic effector (FvNIS1) associated with soybean sudden death syndrome foliar symptoms

Author
item Chang, Hao-xun - University Of Illinois
item Domier, Leslie
item Radwin, Osman - University Of Illinois
item Yendrek, Craig - University Of Illinois
item Hudson, Matthew - University Of Illinois
item Hartman, Glen

Submitted to: Molecular Plant-Microbe Interactions
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 10/8/2015
Publication Date: 1/21/2016
Citation: Chang, H., Domier, L.L., Radwin, O., Yendrek, C., Hudson, M., Hartman, G.L. 2016. Identification of multiple phytotoxins produced by Fusarium virguliforme including a phytotoxic effector (FvNIS1) associated with soybean sudden death syndrome foliar symptoms. Molecular Plant-Microbe Interactions. 96:96-108.

Interpretive Summary: Sudden death syndrome (SDS) is one of the most important diseases of soybean in the United States and is caused by a soil-borne fungal pathogen, Fusarium virguliforme. The disease was first observed in Arkansas in 1971, and since has been reported in most soybean-producing states, with a general movement from the southern to the northern states. Toxins produced by the soil-borne fungus cause characteristic foliar disease symptoms. Our research goal was to identify fungal toxins associated with foliar SDS symptoms. Molecular technologies were used to capture genes putatively related to toxin production. Potentially toxic fungal metabolites were identified and their toxicities were assayed on soybean tissues. The fungus was shown to produce two potentially toxic metabolites, radicicol and citrinin, in culture, and this is the first report of citrinin synthesis by this fungus. When expressed in soybean plants from a Soybean mosaic virus expression system seven of the eight candidate toxin-encoding genes produced only mild chlorosis in soybean; however, one toxic protein induced interveinal chlorosis and necrosis, marginal curling of leaflets, and defoliation, very similar to SDS symptoms observed in the field. Our study revealed that one fungal toxin protein was sufficient to induce SDS foliar symptoms. Other toxins from the fungus may contribute to the disease in other ways, but further research is needed to determine their function. This research is important to soybean pathologists, mycologists, and other scientists interested in toxins produced by fungi that affect plant health.

Technical Abstract: Toxins produced by the soil-borne fungus, Fusarium virguliforme, cause foliar symptoms in soybean. The disease in soybean is referred to as soybean sudden death syndrome (SDS). Three toxins produced by the fungus were reported to be associated with SDS foliar symptoms, but none produced identical SDS foliar symptoms when individually tested. Our research goal was to identify any additional fungal toxins associated with foliar SDS symptoms. A RNA-Seq transcriptome was used to capture putative genes related to toxin production at two time points. The candidate toxic metabolites were confirmed by LC/MS/MS and their toxicities were assayed on soybean tissues. Candidate toxic proteins were expressed by a Soybean mosaic virus expression system on soybean plants. LC/MS/MS confirmed the presence of radicicol and citrinin in the culture filtrate of F. virguliforme. Our study showed that citrinin was synthesized by F. virguliforme, although neither radicicol nor citrinin contributed to SDS foliar symptoms. Most toxic proteins produced only mild chlorosis; however, a toxic protein FvNIS1 induced interveinal chlorosis and necrosis, marginal curling of leaflets, and defoliation. Our study revealed SDS foliar symptoms were induced by FvNIS1 alone. It is possible that other toxins of F. virguliforme contribute to the disease in other ways, but further research is needed to determine their function.