Abstract

Abstract Objectives Rhizopus stolonifer, which causes soft rot of sweet potato, has resulted in substantial loss of economy postharvest. Materials and Methods The antifungal effect and mechanism of cinnamaldehyde (CIN) against R. stolonifer were explored by biochemical analysis and RNA-sequencing in this research, and the edible quality of CIN-treated sweet potato was evaluated. Results The results showed that CIN inhibited the growth of R. stolonifer and reduced the incidence of soft rot in sweet potato at a minimum inhibitory concentration of 1000 μL/L. The damage of the cell walls of R. stolonifer by CIN was associated with the upregulation of CHT1. Cytosolic leakage and malondialdehyde content increased following CIN-treatment, which was correlated with increased reactive oxygen species levels and decreased catalase activity. Upregulation of ERG genes and oxidative stress-related genes following CIN treatment was associated with impaired cell membrane integrity. The mitochondrial structure of R. stolonifer was damaged by CIN treatment resulting in decreased respiration rates and ATP production, which was correlated with lower expression levels of IDH1, COX4, and QCR7. Conclusions Our research suggests that the inhibition of CIN on R. stolonifer was related to the disruption of its normal gene expression network, and CIN maintained the nutritional and edible quality of sweet potato. This study provides valuable insights into the antifungal mechanism of CIN on R. stolonifer and the maintenance of root quality, which contributes to the efficient use of CIN for controlling soft rot in sweet potato.

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