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Reveals enhanced tomato disease resistance through synthetic beneficial microbial communities, suggesting a novel agricultural intervention.
Tomato leaf mold disease, caused by Cladosporium fulvum Cooke, has led to substantial economic losses in agricultural production. When plants are infected by pathogens, they can recruit beneficial microbes to combat infections by phytopathogen. The objective of this project was to construct a synthetic community based on the recruited beneficial microbes for use in controlling tomato leaf mold disease. The composition and structure of the root and rhizosphere microbial communities showed significant differences between tomato plants affected by mild and severe leaf mold disease. Tomato plants with severe leaf mold disease recruited certain beneficial bacterial taxa, such as Enterobacter, Streptomyces, Sphingomonas , and Stenotrophomonas, to the rhizosphere and roots. The synthetic bacterial community I (SC-I), assembled from 11 rhizosphere-enriched strains isolated from tomatoes suffering from severe leaf mold disease, effectively controlled the disease. Based on the rhizosphere and roots colonization capacity, a simplified synthetic bacterial community II (SC-II) composed of seven selected strains maintained its original disease control efficacy. Furthermore, SC-II enhanced plant defense-related enzyme activities, increasing lipoxygenase (LOX), peroxidase (POD), polyphenol oxidase (PPO), and phenylalanine ammonia-lyase (PAL) activities to 1.02-, 1.25-, 1.60-, and 1.28-fold of the control levels, respectively. It also promoted the accumulation of salicylic acid (SA) and jasmonic acid (JA), with peak levels reaching 896.67 pmol/L and 2614.13 pmol/L, respectively, thereby inducing plant resistance against Cladosporium fulvum Cooke infection. Our findings indicate that tomato plants affected by severe leaf mold disease enriched certain beneficial rhizosphere bacteria and constructed a synthetic bacterial community capable of effectively controlling leaf mold disease by inducing resistance against Cladosporium fulvum Cooke infection.
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Mu et al. (2026) studied this question.
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