Knowledge of genetic variations can provide clues into the molecular mechanisms regulating key crop traits. Sweet potato (Ipomoea batatas (L.) Lam.) is an important starch-producing crop, but little is known about the genetic variations in starch biosynthesis and sucrose metabolism genes. Here, we used high-throughput sequencing of pooled amplicons of target genes to identify sequence variations in 20 genes encoding key enzymes involved in starch biosynthesis and sucrose metabolism in 507 sweet potato germplasms. After filtering potential variations between gene copies within the genome, we identified 622 potential allelic single nucleotide polymorphisms (SNPs) and 85 insertions/deletions (InDels), including 50 non-synonymous SNPs (nsSNPs) and 12 frameshift InDels. Three nsSNPs were confirmed to be present in eight sweet potato varieties with various starch properties using cleaved amplified polymorphic sequence (CAPS) markers. Gene copy with loss of the fifth intron was detected in IbAGPb3 genes, and loss of multiple introns were observed in IbGBSS1-1 genes and various among germplasms based on intron length polymorphism (ILP) markers. Thus, we identified sequence variations between germplasms in 20 genes involved in starch biosynthesis and sucrose metabolism, and demonstrated the diversity in intron-loss alleles among sweet potato germplasms. These findings provide critical genetic information and useful molecular markers for revealing regulatory mechanism of starch properties.

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.

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