Summary auto-generated
This study investigated why Trichoderma harzianum, a biocontrol fungus effective against Fusarium oxysporum in vivo, cannot parasitize this pathogen in vitro, unlike its demonstrated mycoparasitism against Rhizoctonia solani, Pythium aphanidermatum, and Sclerotium rolfsii. Two T. harzianum strains were examined for their ability to produce lytic enzymes (1,3-β-glucanase and chitinase) and degrade fungal cell walls. Both strains produced these enzymes when grown on various carbon sources, including fungal cell walls. However, when the enzymes were tested against different fungal cell walls, they effectively degraded R. solani and S. rolfsii walls but showed minimal activity against F. oxysporum walls. Treatment of F. oxysporum cell walls with 2 M-NaOH or proteolytic enzymes (protease and trypsin) significantly increased enzyme-mediated monomer release, whereas these treatments had minimal effect on other fungi tested. This suggests that protein or protein-like components in F. oxysporum cell walls render them resistant to enzymatic degradation. The findings indicate that F. oxysporum's biocontrol by T. harzianum likely involves mechanisms other than mycoparasitism, such as competition or antibiosis.
Key findings
- T. harzianum strains T-35 and T-203 failed to parasitize Fusarium oxysporum colonies in vitro despite producing lytic enzymes, unlike their demonstrated mycoparasitism against R. solani, P. aphanidermatum, and S. rolfsii
- Both T. harzianum strains successfully induced and released 1,3-β-glucanase and chitinase when grown on laminarin, chitin, or fungal cell walls as sole carbon sources
- Lytic enzymes from T. harzianum were significantly more effective at degrading R. solani and S. rolfsii cell walls than F. oxysporum cell walls, with minimal monomer release from living F. oxysporum mycelium
- Pretreatment of F. oxysporum cell walls with NaOH or proteolytic enzymes (protease, trypsin) increased susceptibility to enzyme degradation up to 13-fold, suggesting protein-mediated resistance mechanism
- F. oxysporum cell walls contain a proteinaceous barrier layer that protects against enzymatic lysis, indicating that biocontrol of this pathogen by T. harzianum operates through mechanisms other than direct mycoparasitism
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Abstract
SUMMARY: In in vitro tests, two strains of Trichoderma harzianum failed to parasitize colonies of Fusarium oxysporum f. sp. vasinfectum and F. oxysporum f. sp. melonis. However, these strains were strongly mycoparasitic on Rhizoctonia solani and Pythium aphanidermatum. When grown in liquid cultures containing laminarin, chitin or fungal cell walls as sole carbon sources, both strains of T. harzianum released, 3-β-glucanase and chitinase into the medium. Higher levels of these enzymes were induced in strain T-203 than in T-35 by hyphal cell walls of F. oxysporum. When the lytic enzymes produced by T-35 were incubated with hyphal cell walls of the test fungi, more glucose and N-acetyl-d-glucosamine was released from cell walls of R. solani and Sclerotium rolfsii than from those of F. oxysporum. Treatment of F. oxysporum cell walls with 2 m-NaOH, protease or trypsin prior to their incubation with the lytic enzymes of T. harzianum significantly increased the release of glucose and N-acetyl-d-glucosamine. The effect of these treatments on R. solani and S. rolfsii cell walls was much lower. These results suggest that proteins in the cell walls of F. oxysporum may make these walls more resistant than those of R. solani or S. rolfsii to degradation by extracellular enzymes of T. harzianum.