Anthracnose is a destructive postharvest disease of mango fruit, especially after ripening. The application of antagonistic Bacillus spp. strains is one of many promising control strategies. B. amyloliquefaciens (PMB04) exhibits strong antagonistic activity against anthracnose in strawberry fruit, yet has not been explored for anthracnose control in mango fruit. Among seven tested rhizobacterial strains, PMB04 exhibited the strongest inhibition against Colletotrichum gloeosporioides (Cg) growth. PMB04 demonstrated better inhibitory activity against Cg mycelial growth than the fungicides pyraclostrobin and difenoconazole. A PMB04 fermentation broth (PMB04FB) was prepared and tested, and showed superior efficacy in the reduction of anthracnose disease severity in mangoes compared to a PMB04 suspension, difenoconazole, or pyraclostrobin. We further found PMB04FB increased the mortality ratio of Cg conidia. Our study demonstrates that treatment with PMB04FB is an effective control method for anthracnose in mango and represents a promising strategy for postharvest mango processing.

When a plant is infected by a pathogen, endogenous immune responses are initiated. When the initiation of these defense responses is induced by a pathogen-associated molecular pattern (PAMP) of a pathogen, it is called PAMP-triggered immunity (PTI). Previous studies have shown that Bacillus amyloliquefaciens PMB05 can enhance PTI signals and improve disease control of bacterial soft rot and wilt in Arabidopsis thaliana. In the context of controlling bacterial wilt disease, the involvement of a mitogen-activated protein kinase (MAPK) signaling pathway has been established. Nevertheless, it remains unclear whether this pathway is also required for B. amyloliquefaciens PMB05 in controlling bacterial soft rot. In this study, A. thaliana ecotype Columbia (Col-0) and its mutants on a MAPK pathway-related pathway were used as a model and established that the ability of B. amyloliquefaciens PMB05 to control soft rot requires the participation of the MAPK pathway. Moreover, the enhancement of disease resistance by PMB05 is highly correlated with the activation of reactive oxygen species generation and stomata closure, rather than callose deposition. The spray inoculation method was used to illustrate that PMB05 can enhance stomatal closure, thereby restricting invasion by the soft rot bacterium. This control mechanism has also been demonstrated to require the activation of the MAPK pathway. This study demonstrates that B. amyloliquefaciens PMB05 can accelerate stomata closure via the activation of the MAPK pathway during PTI, thereby reducing pathogen invasion and achieving disease resistance against bacterial soft rot.