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First published online September 20, 2007; 10.1104/pp.107.103689 Plant Physiology 145:875-889 (2007) © 2007 American Society of Plant Biologists A Proteinaceous Elicitor Sm1 from the Beneficial Fungus Trichoderma virens Is Required for Induced Systemic Resistance in Maize1,[W] 2Department of Plant Pathology and Microbiology, Texas A&M University, College Station, Texas 77843
We have previously shown that the beneficial filamentous fungus Trichoderma virens secretes the highly effective hydrophobin-like elicitor Sm1 that induces systemic disease resistance in the dicot cotton (Gossypium hirsutum). In this study we tested whether colonization of roots by T. virens can induce systemic protection against a foliar pathogen in the monocot maize (Zea mays), and we further demonstrated the importance of Sm1 during maize-fungal interactions using a functional genomics approach. Maize seedlings were inoculated with T. virens Gv29-8 wild type and transformants in which SM1 was disrupted or constitutively overexpressed in a hydroponic system or in soil-grown maize seedlings challenged with the pathogen Colletotrichum graminicola. We show that similar to dicot plants, colonization of maize roots by T. virens induces systemic protection of the leaves inoculated with C. graminicola. This protection was associated with notable induction of jasmonic acid- and green leaf volatile-biosynthetic genes. Neither deletion nor overexpression of SM1 affected normal growth or development of T. virens, conidial germination, production of gliotoxin, hyphal coiling, hydrophobicity, or the ability to colonize maize roots. Plant bioassays showed that maize grown with SM1-deletion strains exhibited the same levels of systemic protection as non-Trichoderma-treated plants. Moreover, deletion and overexpression of SM1 resulted in significantly reduced and enhanced levels of disease protection, respectively, compared to the wild type. These data together indicate that T. virens is able to effectively activate systemic disease protection in maize and that the functional Sm1 elicitor is required for this activity.
1 This work was supported by grants from the U.S. Department of Agriculture National Research Initiative (2003–35316–13861) and the National Science Foundation (IOB0445650) to C.M.K., and a fellowship to S.D. from the Storkan-Hanes-McCaslin Foundation. 2 Present address: Department of Molecular Biology, Massachusetts General Hospital and Department of Genetics, Harvard Medical School, Boston, MA 02114. The author responsible for distribution of materials integral to the findings presented in this article in accordance with the policy described in the Instructions for Authors (www.plantphysiol.org) is: Charles M. Kenerley (c-kenerley{at}tamu.edu). [W] The online version of this article contains Web-only data. www.plantphysiol.org/cgi/doi/10.1104/pp.107.103689 * Corresponding author; e-mail c-kenerley{at}tamu.edu. Received June 10, 2007; accepted September 17, 2007; published September 20, 2007. This article has been cited by other articles:
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