Abstract
Cross-incompatibility, frequently happening in intraspecific varieties, has seriously restricted sweetpotato breeding. However, the mechanism of sweetpotato intraspecific cross-incompatibility (ICI) remains largely unexplored, especially for molecular mechanism. Treatment by inducible reagent developed by our lab provides a method to generate material for mechanism study, which could promote incompatible pollen germination and tube growth in the ICI group. Based on the differential phenotypes between treated and untreated samples, transcriptome and metabolome were employed to explore the molecular mechanism of sweetpotato ICI in this study, taking varieties 'Guangshu 146' and 'Shangshu 19', a typical incompatible combination, as materials. The results from transcriptome analysis showed oxidation-reduction, cell wall metabolism, plant-pathogen interaction, and plant hormone signal transduction were the essential pathways for sweetpotato ICI regulation. The differentially expressed genes (DEGs) enriched in these pathways were the important candidate genes to response ICI. Metabolome analysis showed that multiple differential metabolites (DMs) involved oxidation-reduction were identified. The most significant DM identified in comparison between compatible and incompatible samples was vitexin-2-O-glucoside, a flavonoid metabolite. Corresponding to it, cytochrome P450s were the most DEGs identified in oxidation-reduction, which were implicated in flavonoid biosynthesis. It further suggested oxidation-reduction play an important role in sweetpotato ICI regulation. To validate function of oxidation-reduction, reactive oxygen species (ROS) was detected in compatible and incompatible samples. The green fluorescence was observed in incompatible but not in compatible samples. It indicated ROS regulated by oxidation-reduction is important pathway to response sweetpotato ICI. The results in this study would provide valuable insights into molecular mechanisms for sweetpotato ICI.