Abstract

Black spot disease caused by Ceratocystis fimbriata (C. fimbriata)is a severe postharvest disease of sweet potatoes. This study evaluated the biocontrol potential of Bacillus velezensis (B. velezensis) L33a against this pathogen. Confrontation assays showed that L33a inhibited mycelial growth by 82.83%. FDA/PI staining and scanning electron microscopy revealed that L33a disrupted cell membrane integrity and caused severe mycelial deformation. Co-culture experiments indicated that L33a altered the expression of key pathogenic genes in C. fimbriata. Volatile organic compounds (VOCs) from L33a inhibited the pathogen by 77.78%, outperforming cell-free supernatant (CFS). VOCs primarily suppressed spore germination, with phenylethanol (PEA) and octanoic acid achieving 100% inhibition. In planta tests on sweet potato tubers showed that both L33a culture and VOCs significantly reduced lesion expansion. Using qPCR analysis, we found that L33a activated defense-related genes in tissues around wounds, particularly those involved in the jasmonic acid (JA) signaling pathway. In summary, B. velezensis L33a effectively controls sweet potato black rot through multiple mechanisms: direct antifungal activity, inhibition of spore germination, modulation of pathogen gene expression, and induction of host defense responses. It represents a promising natural inhibitor for postharvest disease management.

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