Silica nanoparticles suppress fungal pathogenic allies to alleviate Astragalus root rot

Biological control mechanisms involve the inhibitory effect of antagonistic bacteria on pathogenic fungal growth. However, research on controlling crop diseases by inhibiting allies of pathogenic agents is relatively scarce.

In this study, the application of SiO₂ NPs resulted in an increase in the alpha diversity of the microbial communities in the rhizosphere of Astragalus, as well as an increase in the complexity of the co-occurrence network. SiO₂ NPs reduced the abundance of Pseudomonas and Microbacterium in the rhizosphere of Astragalus. Co-inoculated Fusarium with Pseudomonas aeruginosa and Microbacterium oxydans could exacerbate the root rot of disease in Astragalus. In addition, M. oxydans SCK-308 and P. aeruginosa XS-134-7 promoted the growth of Fusarium oxysporum and inhibited the growth of certain beneficial rhizosphere microorganisms, thereby facilitating the occurrence of the disease. Metabolomic analyses revealed that salicylic acid, indole-3-acetic acid, brassinosteroid, and palmitic acid were significantly enriched in the rhizosphere of Astragalus treated with SiO₂ NPs. Exogenous supplementation with these metabolites significantly inhibited the growth of P. aeruginosa and M. oxydans, thereby alleviating root rot in plants during coinfection with two bacteria and F. oxysporum. These results indicate that the metabolites enhance disease control efficacy through targeted inhibition of pathogen helpers. Additionally, SiO₂ NPs enhanced the enzymatic activities of ascorbate peroxidase, catalase, and peroxidase in Astragalus plants.

Our findings suggest that SiO₂ NPs alter the composition of the rhizosphere microbial community and reduce the population of allies of F. oxysporum, activating salicylic acid-dependent systemic acquired resistance (SAR) in Astragalus and thereby decreasing the incidence of Fusarium root rot. These results suggest that SiO₂ NPs can serve as a sustainable agricultural practice. Video Abstract.