Ralstonia solanacearum infection induces tobacco root to secrete chemoattractants to recruit antagonistic bacteria and defensive compounds to inhibit pathogen

Abstract BACKGROUND Plant root exudates play crucial roles in maintaining the structure and function of the whole belowground ecosystem and regulating the interactions between roots and soil microorganisms. Ralstonia solanacearum causes bacterial wilt disease in many plants, while root exudate‐mediated inhibition of pathogen infection is poorly understood. Here, we characterize the chemical divergence between root exudates of healthy and diseased tobacco plants and the effects of that variability on the rhizosphere microbial community and the occurrence of bacterial wilt. RESULTS Compared with the healthy plants, root exudates in diseased plants showed distinct exudation patterns and metabolite profiles including increased amounts of flavonoids, phenylpropanoids, terpenoids and defense‐related hormones, as well as distinct bacterial community composition, as illustrated by an increased abundance of Ralstonia and decreased abundances of Bacillus and Streptomyces in diseased plants rhizosphere. Pathogen infection stimulated roots to secrete more defensive compounds to inhibit pathogen growth. Change of root exudates modulated rhizosphere microbial community. Specific root exudates could benefit plants by attracting antagonistic Bacillus amyloliquefaciens and inhibiting pathogens. Bacillus amyloliquefaciens could utilize specific root exudates as carbon sources. Benzyl cinnamatel promoted the biofilm formation and colonization of B. amyloliquefaciens on roots. CONCLUSION To defend against pathogen invasion, tobacco plants recruited antagonistic and plant growth‐promoting rhizobacteria to the rhizosphere by modifying root exudate profiles. Specific signal molecules are recommended to recruit beneficial microorganisms for controlling bacterial wilt. The results provide insights concerning the metabolic divergence of root exudates integral to understanding root‐microorganism interaction. © 2024 Society of Chemical Industry.