Evaluation of Selected Zambian Popular Sweet Potato Genotypes for Response to Sweet Potato Virus Disease

Aim: The objective of this study was to determine the effect of sweet potato virus disease (SPVD) on the beta carotene content, tuber weight and vine weight of selected popular sweet potato genotypes. Study Design: The experiment was laid as a randomized complete block design (RCBD) with three replications. Place and Duration of Study: The experiment was conducted for two cropping seasons (2015/16 and 2016/17) at the Zambia Agriculture Research Institute in Chilanga district of Zambia. Methodology: The uninfected (control) genotypes of Kanga, Chiwoko and Chingovwa were evaluated alongside their SPVD infected genotypes. Genotypic infection was confirmed using molecular approaches, and data was collected at harvest on beta carotene content, tuber weight and vine weight. Results: The results showed that SPVD affects the yield and beta carotene content of sweet potato. Significant differences (P< .001) for yield performance and beta carotene were observed. The yield reduction in percentage across seasons for all genotypes between the uninfected and infected genotypes ranged from 77% to 79% and 67% to 76% for tuber weight and vine weight respectively. Only Chiwoko exhibited higher levels of beta carotene among the genotypes. However, the SPVD infected Chiwoko genotype compared to the uninfected treatment produced mean beta carotene content of 39.1 µg/g and 91.5 µg/g respectively. Conclusion: SPVD reduces the tuber weight, vine weight and beta carotene content in infected sweet potato genotypes.

The Spread and Transmission of Sweet Potato Virus Disease (SPVD) and Its Effect on the Gene Expression Profile in Sweet Potato

Sweet potato virus disease (SPVD) is the most devastating viral disease in sweet potato (Ipomoea batatas (L.) Lam.), causing substantial yield losses worldwide. We conducted a systemic investigation on the spread, transmission, and pathogenesis of SPVD. Field experiments conducted over two years on ten sweet potato varieties showed that SPVD symptoms first occurred in newly developed top leaves, and spread from adjacent to distant plants in the field. The SPVD incidence was mainly (but not only) determined by the resistance of the varieties planted, and each variety exhibited a characteristic subset of SPVD symptoms. SPVD was not robustly transmitted through friction inoculation, but friction of the main stem might contribute to a higher SPVD incidence rate compared to friction of the leaf and branch tissues. Furthermore, our results suggested that SPVD might be latent in the storage root. Therefore, using virus-free storage roots and cuttings, purposeful monitoring for SPVD according to variety-specific symptoms, and swiftly removing infected plants (especially during the later growth stages) would help control and prevent SPVD during sweet potato production. Comparative transcriptome analysis revealed that numerous genes involved in photosynthesis, starch and sucrose metabolism, flavonoid biosynthesis, and carotenoid biosynthesis were downregulated following SPVD, whereas those involved in monolignol biosynthesis, zeatin biosynthesis, trehalose metabolism, and linoleic acid metabolism were upregulated. Notably, critical genes involved in pathogenesis and plant defense were significantly induced or suppressed following SPVD. These data provide insights into the molecular changes of sweet potato in response to SPVD and elucidate potential SPVD pathogenesis and defense mechanisms in sweet potato. Our study provides important information that can be used to tailor sustainable SPVD control strategies and guide the molecular breeding of SPVD-resistant sweet potato varieties.