The involvement of volatile and nonvolatile antibiotics in the antagonism by Trichoderma has been proposed (Dennis and Webster 1971a,b). Indeed some isolates of Trichoderma excrete growth inhibitory substances (Claydon et al. 1987; Ghisalberti and Sivasithamparam 1991; Sivan et al. 1984). Claydon et al. (1987) identified volatile alkyl pyrons produced by T. harzianum that were inhibitory to a number of fungi in vitro. When these metabolites were added to a peat-soil mixture, they reduced the incidence of R. solani-induced damping-off on lettuce. However, there is insufficient evidence to be conclusive about their contribution to pathogen suppression and disease reduction in situ. Trichoderma also produces linear oligopeptides of 12-22 aminoacids (pep-taibols), which are rich in -aminoisobutyric acid, N-acetylated at the N-terminus and containing an amino alcohol at the C-terminus (Rebuffat et al. 1989; 1991). These oligopeptides are known to form voltage-gated ion channels in black lipid membranes and modify the membrane permeability of liposomes (El Hadjji et al. 1989). This suggested a scenario where cell-wall degrading enzymes weaken the cell wall and peptaibol antibiotics inhibit synthesis of cell-wall components, impairing the capacity of the hyphae to repair the effect of cell-wall degrading enzymes (Lorito et al. 1996a,b). This hypothesis is supported by the fact that the action of cellwall degrading enzymes is synergistic with that of antibiotics (Lorito et al. 1996a,b).
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