Abstract Coinfection with sweet potato chlorotic stunt virus (SPCSV) and sweet potato feathery mottle virus (SPFMV) causes sweet potato virus disease, with severe symptoms in sweet potato, decreasing sweet potato yield and root quality. However, the associated molecular mechanisms remain unknown. In this study, changes in mRNA and small RNA (sRNA) expression in storage roots and their 1‐ and 3‐week‐old sprouts infected with SPCSV, SPFMV, or SPCSV + SPFMV were analyzed via RNA sequencing and sRNA sequencing, respectively. The number of differentially expressed genes (DEGs) and differentially expressed microRNAs (DEMs) did not differ significantly between the roots and sprouts infected with only one virus. However, a higher number of DEGs or DEMs were observed in coinfected sprouts than in storage roots or sprouts infected with only one virus. The downregulated genes in coinfected samples were involved in phytohormone biosynthesis and signal transduction (storage roots) as well as photosynthesis, chloroplasts, and chloroplast thylakoid membranes (sprouts). Some defense‐related microRNAs of the miR156, miR164, miR165, and miR171 families were significantly upregulated in coinfected sprouts. Our results also showed that the coinfection increased the accumulation of SPFMV‐derived small interfering RNAs and upregulated the expression of several key genes in the RNA silencing pathway in sprouts. This study provides insights into the molecular basis of the synergistic effects of SPFMV and SPCSV on sweet potato storage roots and their sprouts.
Zhang et al. (Tue,) studied this question.