The conserved global regulator VeA is necessary for symptom production and mycotoxin synthesis in maize seedlings by Fusarium verticillioides

Authors

  • K. Myung,

    1. Department of Biological Sciences, Northern Illinois University, 1425 W. Lincoln Hwy., DeKalb, IL 60115
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    • Current address: Dow AgroSciences LLC, 9330 Zionsville Road, Indianapolis, IN 46268, USA

    • Contributed equally to the work.

  • N. C. Zitomer,

    1. Toxicology and Mycotoxin Research Unit, USDA-ARS, Russell Research Center, Athens, GA 30605, USA
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    • Current address: Nutritional Biomarkers Branch, Division of Laboratory Sciences, National Center for Environmental Health, Centers for Disease Control and Prevention, Atlanta, GA 30341-3724, USA

    • Contributed equally to the work.

  • M. Duvall,

    1. Department of Biological Sciences, Northern Illinois University, 1425 W. Lincoln Hwy., DeKalb, IL 60115
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  • A. E. Glenn,

    1. Toxicology and Mycotoxin Research Unit, USDA-ARS, Russell Research Center, Athens, GA 30605, USA
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  • R. T. Riley,

    1. Toxicology and Mycotoxin Research Unit, USDA-ARS, Russell Research Center, Athens, GA 30605, USA
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  • A. M. Calvo

    Corresponding author
    1. Department of Biological Sciences, Northern Illinois University, 1425 W. Lincoln Hwy., DeKalb, IL 60115
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E-mail: amcalvo@niu.edu

Abstract

The veA or velvet gene is necessary for biosynthesis of mycotoxins and other secondary metabolites in Aspergillus species. In addition, veA has also been demonstrated to be necessary for normal seed colonization in Aspergillus flavus and Aspergillus parasiticus. The present study shows that veA homologues are broadly distributed in fungi, particularly in ascomycetes. The Fusarium verticillioides veA orthologue, FvVE1, is also required for the synthesis of several secondary metabolites, including fumonisin and fusarins. This study also shows that maize plants grown from seeds inoculated with FvVE1 deletion mutants did not show disease symptoms, while plants grown from seeds inoculated with the F. verticillioides wildtype and complementation strains clearly showed disease symptoms under the same experimental conditions. In this latter case, the presence of lesions coincided with accumulation of fumonisins in the plant tissues, and only these plant tissues had elevated levels of sphingoid bases and their 1-phosphate derivatives, indicating inhibition of ceramide synthase and disruption of sphingolipid metabolism. The results strongly suggest that FvVE1 is necessary for pathogenicity by F. verticillioides against maize seedlings. The conservation of veA homologues among ascomycetes suggests that veA could play a pivotal role in regulating secondary metabolism and associated pathogenicity in other fungi.

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