CsNAC29 transcription factor activates α‐farnesene emission to resist gray blight disease in tea plant (Camellia sinensis)

SUMMARY α‐Farnesene is one of the most widely distributed volatile organic compounds (VOCs) in plants, playing a significant role in both flavor formation and defense mechanisms. However, the regulatory mechanisms and physiological functions of α‐farnesene biosynthesis in tea plants remain largely unexplored. In this study, α‐farnesene was identified as a key compound associated with resistance to gray blight disease. We characterized an α‐farnesene synthase gene ( CsAFS2.1 ) and its alternative splicing isoforms ( CsAFS2.2 and CsAFS2.3 ), which were differentially induced upon pathogen infection, with CsAFS2.1 showing the highest level of induction. Through subcellular localization studies, in vitro enzymatic assays, and in vivo functional verification, we demonstrated that all three isoforms catalyze the conversion of farnesyl pyrophosphate (FPP) to α‐farnesene in tea plants. Using an integrative approach that included DNA–protein interaction analysis, gene silencing, gene overexpression, and metabolic profiling, we revealed that the transcription factor CsNAC29 activates α‐farnesene emission by directly regulating the expression of CsAFS2 . Suppression of either CsNAC29 or CsAFS2 significantly reduced α‐farnesene production and compromised the resistance of tea plants to gray blight disease. Our study not only elucidates the molecular mechanisms underlying α‐farnesene‐mediated resistance in tea plants but also proposes a potential pathway for enhancing both aroma and immunity through targeted genetic manipulation.