The pathogen Colletotrichum gloeosporioides causes anthracnose, a serious threat to tea trees around the world, particularly in warm and humid regions. RNA-Seq data have previously indicated NAC transcription factors are involved in anthracnose resistance, but underlying mechanisms remain unclear. The BiFC, Split-LUC, and Co-IP assays validated the interaction between CsbHLH62 and CsNAC17 identified through yeast two-hybrid (Y2H) screening. CsNAC17 or CsbHLH62 overexpression enhanced anthracnose resistance, as well as enhanced levels of H2O2, hypersensitivity, and cell death in Nicotiana benthamiana. The NBS-LRR gene CsRPM1 is regulated by CsNAC17 by binding directly to its promoter (i.e., CACG, CATGTG), while CsbHLH62 facilitates CsNAC17’s binding and increases trascriptional activity of CsRPM1. Additionally, transient silencing of CsNAC17 and CsbHLH62 in tea plant leaves using the virus-induced gene silencing (VIGS) system resulted in decreased resistance to anthracnose. Conversely, transient overexpression of CsNAC17 and CsbHLH62 in tea leaves significantly enhanced the resistance against anthracnose. Based on these results, it appears that CsbHLH62 facilitates the activity of CsNAC17 on CsRPM1, contributing to increased anthracnose resistance.

中文翻译：

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CsNAC17 通过与 CsbHLH62 相互作用增强山茶花对胶孢炭疽菌的抗性


病原体 Colletotrichum gloeosporioides 会导致炭疽病，对世界各地的茶树构成严重威胁，尤其是在温暖潮湿的地区。RNA-Seq 数据先前表明 NAC 转录因子与炭疽病耐药性有关，但潜在机制仍不清楚。BiFC 、 Split-LUC 和 Co-IP 检测验证了通过酵母双杂交 （Y2H） 筛选鉴定的 CsbHLH62 和 CsNAC17 之间的相互作用。CsNAC17 或 CsbHLH62 过表达增强了炭疽病耐药性，以及 H2O2 水平升高、超敏反应和本氏烟草细胞死亡。NBS-LRR 基因 CsRPM1 通过直接与其启动子 （即 CACG、CATGTG） 结合受 CsNAC17 调节，而 CsbHLH62 促进 CsNAC17 的结合并增加 CsRPM1 的转录活性。此外，使用病毒诱导的基因沉默 （VIGS） 系统在茶树叶片中瞬时沉默 CsNAC17 和 CsbHLH62 导致对炭疽病的耐药性降低。相反，茶叶中瞬时过表达 CsNAC17 和 CsbHLH62 显著增强了对炭疽病的抵抗力。基于这些结果，CsbHLH62 似乎促进了 CsNAC17 对 CsRPM1 的活性，有助于增加炭疽病耐药性。