Sclerotia of the plant pathogen Rhizoctonia solani Kühn as a new source of bioactive compounds

Rhizoctonia solani Kühn is a soil-born fungal pathogen that causes economic losses to a large number of crops. The aim of this study is to evaluate the bioactivity of the resistant vegetative structure, the sclerotia. The composition of exudates and extracts of sclerotia of R. solani strains AG2 2111B and AG3 114 respectively, were analyzed by gas chromatography-mass spectrometry [1] and direct infusion mass spectrometry [2]. Sclerotial exudates (3000mg d.w./ml) had a variable inhibitory effect on spore germination of the following fungi: Stachybotrys elegans (70%), Fusarium sporotrichioides (21%) and Trichoderma virens (14%). In addition, the same concentration of exudates was phytotoxic to duckweed (Lemna minor L.) causing a significant reduction in chlorophyll content (31%) and number of fronts (34%). Mass spectrometry analysis revealed the complexity of exudates' composition and the presence of several substances including carboxylic acids, quinones, carbohydrates and fatty acids. On the other hand, the extracts of sclerotia of R. solani strain 114 were phytotoxic to potato seedlings. The fraction responsible for the observed phytotoxicity was isolated by thin layer chromatography and analyzed by gas chromatography-mass spectrometry [1] and direct infusion mass spectrometry [2]. The results revealed that dibutyl phthalate is the main bioactive compound of the fraction responsible for the observed toxicity which has also been reported as a bioactive compound in other fungal pathogens [3]. This is the first report describing the composition and phytotoxicity of R. solani sclerotial extracts and exudates.

Acknowledgements: Department of Food Science, McGill University 1, Mass Spectrometry Unit, McGill University and Génome Québec Innovation Centre 2, Dr W. D. Marshall 1, Dr O.A. Mamer 2

References: 1. Börner, J. et al. (2007) Anal. Chem. 367: 143–151.

2. Smedsgaard, J., Nielsen, L. (2005)J. Exp. Bot. 56: 276–286.

3. Roy, R. et al. (2006) Microbiol. Res. 161: 121–126.