4.7 Article

Biological control of Monilinia laxa and Rhizopus stolonifer in postharvest of stone fruit by Pantoea agglomerans EPS125 and putative mechanisms of antagonism

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DOI: 10.1016/S0168-1605(02)00403-8

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stone fruit rot; dose-response; biocontrol agent-pathogen interaction; Pantoea agglomerans; bacterial biocontrol agent; post-harvest disease

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Treatment of stone fruits (apricot, peach and nectarine) with Pantoea agglomerans strain EPS125 decreased the incidence and diameter of lesions of brown rot caused by Monilinia laxa and soft rot caused by Rhizopus stolonifer. Root control was achieved on fruits either wounded and subsequently inoculated with the pathogens or non-wounded and naturally infected from orchards. The efficacy of biocontrol was dependent on the concentration of the biocontrol agent and pathogen. At medium to low pathogen dose, optimal EPS125 concentrations were above 10(7) CFU ml(-1). The median effective dose (ED50) of EPS125 was 4.5 x 10(4) in M. laxa and 2.2 x 10(5) CFU ml(-1) in R. stolonifer. However, EPS125 was more effective in M. lava than in R. stolonifer as indicated by the ratio between ED50 of the biocontrol agent and pathogen (K-z/K-x) which was 166 and 1263, respectively. Interactions between the strain EPS125 and the fruit surface, and M. laxa and R. stolonifer, were studied to determine the mechanisms of protection from postharvest rots. The strain EPS125 colonizes, grows and survives on stone fruit wounds. Significant inhibition of conidial germination and hyphal growth of R. stolonfer and M laxa was achieved when the fungal and EPS125 cells were cocultivated on peel leachate or nectarine juice. However, no effect was observed when the antagonist and the pathogen cells were physically separated by a membrane filter which permits nutrient and metabolite interchange. Therefore, a direct interaction between the strain and the pathogen cells is necessary for antagonism, without a significant contribution of the production of antibiotic substances or nutrient competition. Preemptive exclusion by wound colonization and direct interaction with the pathogen is proposed as the mechanism of biocontrol. (C) 2002 Elsevier Science B.V All rights reserved.

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