Water-deficit stress reprograms flavan-3-ol biosynthesis toward gallocatechin through a TgERF23–TgLAR1 module in Torreya grandis

Water-deficit stress disrupts redox homeostasis in plants, yet how flavan-3-ol biosynthesis is reprogrammed to bolster antioxidant defense remains elusive. By integrating physiological assays, metabolite profiling, transcriptomics, and transient functional analyses in Torreya grandis , this study demonstrated that water-deficit stress redirects metabolic flux toward gallocatechin, which comprises up to 65% of the quantified flavan-3-ol pool. TgLAR1 was identified as the principal leucoanthocyanidin reductase mediating this response: TgLAR1 overexpression increased gallocatechin levels and antioxidant enzyme activities, whereas virus-induced silencing diminished both. Transcriptome mining revealed that the APETALA2/ethylene-responsive factor (AP2/ERF) transcription factor TgERF23 directly binds a GCC-box motif in the TgLAR1 promoter to activate transcription. TgERF23 overexpression upregulated TgLAR1 , promoted gallocatechin accumulation, and enhanced antioxidant capacity. Conversely, TgERF23 silencing suppressed this cascade. Together, these findings establish a TgERF23–TgLAR1 regulatory module that directs branch-preferential reprogramming of flavan-3-ol metabolism toward gallocatechin under water-deficit stress. This work provides a mechanistic framework for understanding stress-responsive specialized metabolism and identifying candidate genes to improve water-deficit adaptation in woody gymnosperms.