Abstract

Sweet potato (Ipomoea batatas L.) is a nutritionally valuable crop whose postharvest quality is seriously affected by Rhizopus soft rot. This study aimed to isolate and characterize the causal agent associated with soft rot symptoms in postharvest sweet potato roots and to evaluate its physiological characteristics. Two fungal strains (RS01 and RS02) were isolated from diseased sweet potatoes collected in Hanoi, Vietnam. Of the two strains, strain RS02 exhibited denser, cottony colonies with white-to grey aerial mycelia compared to strain RS01. Pathogenicity assays confirmed that strain RS02 reproduced typical soft rot symptoms and fulfilled Koch’s postulates, with faster disease progression observed on sweet potato slices due to increased exposure of nutrient-rich tissues. Molecular identification based on internal transcribed spacer rDNA further confirmed strain RS02 as Rhizopus stolonifer isolate RS02. Fungal growth was affected by culture medium, temperature, pH, and carbon sources. This isolate grew rapidly on potato dextrose agar at 25–30°C, pH 4–5, and in the presence of glucose. The isolate also produced extracellular cellulase and pectinase, suggesting a role of cell wall-degrading enzymes in host tissue maceration. This study links physiological characteristics with postharvest infection biology of R. stolonifer and provides data on environmental and nutritional factors affecting the development of sweet potato soft rot in Vietnam. The findings enhance understanding of fungal adaptation under tropical storage conditions and may support the development of effective postharvest disease management strategies.

Key words: Fungal growth, postharvest storage, Rhizopus soft rot, Rhizopus stolonifer, sweet potato.