RESUMO
Fusarium solani is the main pathogenic fungus causing the root rot of wolfberry (Lycium barbarum). The endophytic fungus Metarhizium robertsii has been widely used for the biocontrol of plant pathogenic fungi, but the biocontrol effects of this fungus on wolfberry root rot and its antifungal mechanism against F. solani have not been reported. In this study, the antagonism of endophytic fungus M. robertsii against F. solani was verified. Further, we optimized the fermentation conditions of M. robertsii fermentation broth based on the inhibition rate of F. solani. In addition, the effects of M. robertsii fermentation broth on the root rot of wolfberry and its partial inhibition mechanism were investigated. The results showed that M. robertsii exhibited good antagonism against F. solani. Glucose and beef extracts were the optimal carbon and nitrogen sources for the fermentation of M. robertsii. Under the conditions of 29 °C, 190 rpm, and pH 7.0, the fermentation broth of M. robertsii had the best inhibition effect on F. solani. Furthermore, the fermentation broth treatment decreased the activities of superoxide dismutase, catalase, and peroxidase of F. solani; promoted the accumulation of malondialdehyde; and accelerated the leakage of soluble protein and the decrease in soluble sugar. In addition, inoculation with M. robertsii significantly reduced the decay incidence and disease index of wolfberry root rot caused by F. solani. These results indicate that M. robertsii could be used as a biological control agent in wolfberry root rot disease management.
RESUMO
Fusarium solani is one of the primary pathogens causing root rot of wolfberry. The aims of this study were to investigate the inhibitory effect of potato glycoside alkaloids (PGA) on F. solani and its energy metabolism. In this study, the effects of PGA treatment on the growth and development of F. solani were investigated and the changes in the glycolytic pathway (EMP), ATPase activity, mitochondrial complex activity, mitochondrial structure, and energy charge level were analyzed to elucidate the possible antifungal mechanism of PGA on F. solani. The results showed that PGA treatment inhibited the colony growth, biomass, and spore germination of F. solani. PGA treatment reduced the glucose content and Hexokinase (HK) activity of F. solani, but increased the activity of Fructose-6-Phosphate Kinase (PFK) and Pyruvate Kinase (PK) and promoted the accumulation of pyruvic acid. In addition, PGA treatment inhibited the activities of H+-ATPase, Ca2+-ATPase, and mitochondrial complex IV, increased the mitochondrial inner membrane Ca2+ content and mitochondrial membrane permeability transition pore, and decreased the contents of ATP, ADP, and AMP as well as the energy charge. These results indicate that PGA treatment inhibits the growth and development of F. solani, activates the glycolysis pathway, inhibits ATPase activity and mitochondrial complex activity, and destroys the structure and function of mitochondrial membrane, resulting in a lower energy charge level.