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CsNAC29转录因子激活α-法尼烯排放以抵抗茶树(Camellia sinensis)的灰枯病。

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

作者信息

Xu Qingshan, Zhuang Zinan, Cheng Long, Jin Jiayi, Ma Huicong, Chen Huirui, Xiang Wen, Wang Xinyu, Zhao Ziyan, Zhu Junyan, Liu Shuyuan, Yu Youben

机构信息

College of Horticulture, Northwest A&F University, Yangling, Shaanxi, 712100, China.

State Key Laboratory of Tea Plant Biology and Utilization, Anhui Agricultural University, West 130 Changjiang Road, Hefei, Anhui, 230036, China.

出版信息

Plant J. 2025 Aug;123(3):e70421. doi: 10.1111/tpj.70421.

DOI:10.1111/tpj.70421
PMID:40795236
Abstract

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.

摘要

α-法尼烯是植物中分布最广泛的挥发性有机化合物(VOCs)之一,在风味形成和防御机制中都发挥着重要作用。然而,茶树中α-法尼烯生物合成的调控机制和生理功能在很大程度上仍未被探索。在本研究中,α-法尼烯被鉴定为与抗灰斑病相关的关键化合物。我们对一个α-法尼烯合酶基因(CsAFS2.1)及其可变剪接异构体(CsAFS2.2和CsAFS2.3)进行了表征,它们在病原体感染后被差异诱导,其中CsAFS2.1的诱导水平最高。通过亚细胞定位研究、体外酶活性测定和体内功能验证,我们证明这三种异构体都能催化茶树中焦磷酸法尼酯(FPP)转化为α-法尼烯。使用包括DNA-蛋白质相互作用分析、基因沉默、基因过表达和代谢谱分析在内的综合方法,我们发现转录因子CsNAC29通过直接调节CsAFS2的表达来激活α-法尼烯的释放。抑制CsNAC29或CsAFS2都会显著降低α-法尼烯的产生,并削弱茶树对灰斑病的抗性。我们的研究不仅阐明了茶树中α-法尼烯介导的抗性的分子机制,还提出了一条通过靶向基因操作增强香气和免疫力的潜在途径。

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