Abstract

Edetate salts are a kind of food additive regarded as candidates for chemical fungicides because of their lower toxicity and higher safety for the environment and human health. The antifungal activities of edetate salts have been determined in some phytopathogens except Penicillium digitatum, which causes the most destructive fungal disease during the citrus postharvest period. In the present study, we investigated the molecular mechanisms of calcium disodium edetate (EDTA-Na2Ca) against P. digitatum in deepth. The results suggested that EDTA-Na2Ca inhibited the P. digitatum P44 strain in vitro at a minimum inhibitory/fungicidal concentration (MIC/MFC) of 50 mmol L−1. Meanwhile, EDTA-Na2Ca also inhibited P. digitatum in vivo by enhancing the host defense system. The P44 strain treated with EDTA-Na2Ca displayed a delayed conidial germination rate, expanded hyphal tips, thickened septa and cell walls, and destroyed mitochondria. Transcriptome sequencing and qRT-PCR analyses indicated that EDTA-Na2Ca suppressed the P44 strain primarily by disturbing the carbohydrate metabolism pathway, especially the synthesis of pyruvate in glycolysis. In addition, the adverse effects, including those on mycelial growth, pyruvate synthesis and superoxide dismutase activity, of EDTA-Na2Ca could be reversed by exogenous Mn2+, implying that Mn2+ chelation is an essential mode of action. In summary, the current work verifies that EDTA-Na2Ca is a potential antifungal drug that cures citrus green mold probably by chelating Mn2+ and targeting pyruvate synthesis in P. digitatum.

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