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Sm1, a Proteinaceous Elicitor Secreted by the Biocontrol Fungus Trichoderma virens Induces Plant Defense Responses and Systemic Resistance

August 2006 , Volume 19 , Number  8
Pages  838 - 853

Slavica Djonović , 1 Maria J. Pozo , 2 Lawrence J. Dangott , 3 Charles R. Howell , 4 and Charles M. Kenerley 1

1Department of Plant Pathology and Microbiology, Texas A&M University, College Station, TX 77843, U.S.A.; 2Department of Soil Microbiology and Symbiotic Systems, Estación Experimental del Zaidín, CSIC, 18008 Granada, Spain; 3Department of Biochemistry and Biophysics, Texas A&M University, College Station; 4USDA-ARS Southern Plains Agricultural Research Center, College Station, TX 77845, U.S.A.

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Accepted 26 March 2006.

The soilborne filamentous fungus Trichoderma virens is a biocontrol agent with a well-known ability to produce antibiotics, parasitize pathogenic fungi, and induce systemic resistance in plants. Even though a plant-mediated response has been confirmed as a component of bioprotection by Trichoderma spp., the molecular mechanisms involved remain largely unknown. Here, we report the identification, purification, and characterization of an elicitor secreted by T. virens, a small protein designated Sm1 (small protein 1). Sm1 lacks toxic activity against plants and microbes. Instead, native, purified Sm1 triggers production of reactive oxygen species in monocot and dicot seedlings, rice, and cotton, and induces the expression of defense-related genes both locally and systemically in cotton. Gene expression analysis revealed that SM1 is expressed throughout fungal development under different nutrient conditions and in the presence of a host plant. Using an axenic hydroponic system, we show that SM1 expression and secretion of the protein is significantly higher in the presence of the plant. Pretreatment of cotton cotyledons with Sm1 provided high levels of protection to the foliar pathogen Colletotrichum sp. These results indicate that Sm1 is involved in the induction of resistance by Trichoderma spp. through the activation of plant defense mechanisms.

© 2006 The American Phytopathological Society