State Key Laboratory of Tea Plant Biology and Utilization, Anhui Agricultural University, Hefei, Anhui, China.
Plant J. 2021 May;106(3):862-875. doi: 10.1111/tpj.15203. Epub 2021 Mar 26.
Gray blight (GB) is one of the most destructive diseases of tea plants, causing considerable damage and productivity losses; however, the dynamic roles of defense genes during pathogen infection remain largely unclear. To explore the numerous molecular interactions associated with GB stress in tea plants, we employed transcriptome, sRNAome and degradome sequencing from 1 to 13 days post-inoculation (dpi) at 3-day intervals. The transcriptomics results showed that differentially expressed genes (DEGs) related to flavonoid synthesis, such as chalcone synthase (CHS) and phenylalanine ammonia-lyase (PAL), were particularly induced at 4 dpi. Consistent with this, the contents of catechins (especially gallocatechin), which are the dominant flavonoids in tea plants, also increased in the leaves of tea plants infected with GB. Combined analysis of the sRNAome and degradome revealed that microRNAs could mediate tea plant immunity by regulating DEG expression at the post-transcriptional level. Co-expression network analysis demonstrated that miR530b-ethylene responsive factor 96 (ERF96) and miRn211-thaumatin-like protein (TLP) play crucial roles in the response to GB. Accordingly, gene-specific antisense oligonucleotide assays suggested that suppressing ERF96 decreased the levels of reactive oxygen species (ROS), whereas suppressing TLP increased the levels of ROS. Furthermore, ERF96 was induced, but TLP was suppressed, in susceptible tea cultivars. Our results collectively demonstrate that ERF96 is a negative regulator and TLP is a positive regulator in the response of tea plants to GB. Taken together, our comprehensive integrated analysis reveals a dynamic regulatory network linked to GB stress in tea plants and provides candidate genes for improvement of tea plants.
灰斑病（GB）是茶树最具破坏性的病害之一，导致相当大的损害和生产力损失；然而，防御基因在病原体感染过程中的动态作用在很大程度上仍不清楚。为了探索与茶树 GB 胁迫相关的众多分子相互作用，我们采用转录组、sRNAome 和降解组测序技术，每隔 3 天从接种后 1 天到 13 天（dpi）进行测序。转录组学结果表明，与类黄酮合成相关的差异表达基因（DEGs），如查尔酮合酶（CHS）和苯丙氨酸解氨酶（PAL），在 4 dpi 时特别被诱导。与此一致，在感染 GB 的茶树叶片中，儿茶素（特别是表没食子儿茶素没食子酸酯）的含量也增加了。sRNAome 和降解组的综合分析表明，microRNAs 可以通过在转录后水平调节 DEG 的表达来介导茶树的免疫。共表达网络分析表明，miR530b-乙烯响应因子 96（ERF96）和 miRn211-类硫蛋白（TLP）在对 GB 的反应中起着关键作用。相应地，基因特异性反义寡核苷酸测定表明，抑制 ERF96 降低了活性氧（ROS）的水平，而抑制 TLP 增加了 ROS 的水平。此外，在易感茶树品种中，ERF96 被诱导，而 TLP 被抑制。我们的研究结果表明，ERF96 是茶树对 GB 反应的负调节因子，而 TLP 是正调节因子。总之，我们的综合分析揭示了一个与茶树 GB 胁迫相关的动态调控网络，并为改良茶树提供了候选基因。
