Comprehensive mechanisms of epigallocatechin-3-gallate (EGCG) metabolism during tea dieback disease infection in tea plant (Camellia sinensis)

Tea dieback is a prevalent disease affecting large-leaf tea plants and significantly impacts the formation of quality components in tea. We isolated and identified the tea dieback pathogen Fusarium proliferatum from the tender shoots of the 'Yinghong 9' tea plant, confirming its ability to decompose (−)-epigallocatechin-3-gallate (EGCG) into (−)-epigallocatechin (EGC) and gallic acid (GA). To evaluate differentially expressed genes associated with EGCG production in the tender shoots at different stages of tea dieback disease infection, transcriptome analysis was carried out. Our results demonstrated that the inhibition of EGCG synthesis during the later stages is a critical factor contributing to the reduction in EGCG content. Additionally, we obtained the recombinant protein of 2-hydroxyisoflavanone dehydratase-like through gene cloning and prokaryotic expression, which exhibits the ability to decompose EGCG into EGC and GA. This study analyzes the multiple mechanisms by which tea dieback infection regulates EGCG metabolism.