Sweet potato provides rich nutrients and bioactive substances for the human diet. In this study, the volatile organic compounds of five pigmented-fleshed sweet potato cultivars were determined, the characteristic aroma compounds were screened, and a correlation analysis was carried out with the aroma precursors. In total, 66 volatile organic compounds were identified. Terpenoids and aldehydes were the main volatile compounds, accounting for 59% and 17%, respectively. Fifteen compounds, including seven aldehydes, six terpenes, one furan, and phenol, were identified as key aromatic compounds for sweet potato using relative odor activity values (ROAVs) and contributed to flower, sweet, and fat flavors. The OR sample exhibited a significant presence of trans-β-Ionone, while the Y sample showed high levels of benzaldehyde. Starch, soluble sugars, 20 amino acids, and 25 fatty acids were detected as volatile compounds precursors. Among them, total starch (57.2%), phenylalanine (126.82 ± 0.02 g/g), and fatty acids (6.45 μg/mg) were all most abundant in Y, and LY contained the most soluble sugar (14.65%). The results of the correlation analysis revealed the significant correlations were identified between seven carotenoids and trans-β-Ionone, soluble sugar and nerol, two fatty acids and hexanal, phenylalanine and 10 fatty acids with benzaldehyde, respectively. In general, terpenoids and aldehydes were identified as the main key aromatic compounds in sweet potatoes, and carotenoids had more influence on the aroma of OR than other cultivars. Soluble sugars, amino acids, and fatty acids probably serve as important precursors for some key aroma compounds in sweet potatoes. These findings provide valuable insights for the formation of sweet potato aroma.

Postharvest disease is an important limiting factor for sweetpotato production. Recently, a new green mold disease was found in sweetpotato storage roots. To investigate the mechanism underlying the pathogenesis of the disease, the pathogen was isolated and identified based on morphological and molecular features, and its characteristics were further analyzed by pathogenic and antagonistic evaluations. The results showed that the isolated pathogen (CRI-Ta1) was identified as Trichoderma asperellum based on the similar growth and morphological features with Trichoderma spp., 99% homology of internal transcribed spacer (ITS) sequence, and membership to the same phylogenetic group with the model strain of T. asperellum (CBS 433.97). The pathogenic analysis revealed that CRI-Ta1 could cause green mold disease through wound infection on the storage roots and the strains reisolated from infected storage roots could cause disease in different sweetpotato varieties, which was fulfilled in Koch’s postulate. Moreover, CRI-Ta1 could also infect other common crop species, including chestnut, carrot, apple, pear, and others. It indicated that CRI-Ta1 was the pathogen to the storage roots of sweetpotato and had a wide host range. Additionally, in vitro antagonistic evaluation showed that CRI-Ta1 effectively inhibited the growth of common sweetpotato pathogens, including Fusarium solani and Rhizopus nigricans. However, further research is needed on the potential of CRI-Ta1 to control sweetpotato diseases in vivo. Collectively, our findings provided valuable insights into the characteristics of the T. asperellum CRI-Ta1 in sweetpotato and would be helpful to the prevention and control of sweetpotato green mold disease.

Phosphorus deficiency poses a significant challenge to the growth and productivity of crops, particularly in nutrient-poor soils. This study investigates the effects of phosphorus deficiency on the growth, endogenous phytohormones, metabolome, and transcriptome of sweet potato (Ipomoea batatas L.) over a growth period from 30 to 120 days. We found that low phosphorus conditions significantly reduced both above- and below-ground biomass, while tuber number remained unchanged. Endogenous phytohormone analysis revealed altered levels of abscisic acid (ABA), indole-3-acetic acid (IAA), and cytokinins, indicating a complex hormonal response to phosphorus starvation. Transcriptomic analysis identified a total of 6324 differentially expressed genes (DEGs) at 60 days, with significant enrichment in pathways related to stress response and phosphorus utilization (PAPs and PHO1). Metabolomic profiling revealed notable shifts in key metabolites, with consistent downregulation of several phosphorous-related compounds. Our findings highlight the intricate interplay between growth, hormonal regulation, metabolic reprogramming, and gene expression in response to phosphorus deficiency in sweet potato. This research underscores the importance of understanding nutrient stress responses to enhance sweet potato resilience and inform sustainable agricultural practices. Future research should focus on exploring the potential for genetic and agronomic interventions to mitigate the effects of phosphorus deficiency and optimize sweet potato productivity in challenging environments.