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Biocontrol of postharvest soft rot caused by Rhizopus stolonifer in sweet potatoes using volatile organic compounds from actinomycete Nocardiopsis dassonvillei MI-S24

Journal 2025 · IF 6.3 · 发表于 2025 年 4 月 11 日
作者: Abd El-Rahman F Gomaa,Jing Tao,Sun-Yan Liang,Jia-Qi Liu,Si Yang,Xiao-Qiong Shi,Mohamed H. El-Sayed,Ke Xing,Sheng Qin
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摘要

Root rot caused by Rhizopus stolonifer significantly diminished the yield and quality of sweet potatoes. Currently, the control of root rot predominantly relied on toxic chemical pesticides, with a notable lack of effective alternative strategies. Microbial volatile organic compounds (VOCs) are regarded as an environmentally friendly and safe method for controlling postharvest diseases. This study investigated the in vitro and in vivo effects of VOCs produced by the Nocardiopsis dassonvillei MI-S24 strain against R. stolonifer . The results demonstrated that VOCs exhibit strong antifungal activity against various pathogenic fungi. They significantly inhibited hyphal growth (91.85 %) and spore germination of R. stolonifer while inducing morphological changes. Furthermore, during storage at 28 °C for 20 days, VOCs fumigation effectively mitigated the incidence of postharvest sweet potato root rot. It enhanced the activity of CAT, POD, SOD, PPO, and PAL enzymes by 84.62 %, 38.19 %, 47.98 %, 84.52 %, and 19.50 % respectively in sweet potatoes, safeguarded soluble sugars and starch from degradation, and preserved overall quality. Analysis of volatile components coupled with antifungal validation revealed that 2-methyl-3-(methylthio) furan and 2-undecanol exhibited significant antifungal activity against R. stolonifer . Further research indicated that VOCs affected cell membrane integrity in R. stolonifer , stimulated reactive oxygen species (ROS) accumulation, reduced antioxidant enzyme activity, elevated malondialdehyde levels, induced oxidative damage, and disrupted ATP synthesis as well as TCA cycle processes by diminishing mitochondrial membrane potential alongside succinate dehydrogenase activity, ultimately leading to mitochondrial dysfunction. This study presents a novel biological strategy aimed at preventing and controlling soft rot disease in postharvest sweet potatoes.

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