Yan Shuangshuang, Wang Yixi, Yu Bingwei, Gan Yuwei, Lei Jianjun, Chen Changming, Zhu Zhangsheng, Qiu Zhengkun, Cao Bihao
Key Laboratory of Biology and Genetic Improvement of Horticultural Crops, Ministry of Agriculture and Rural Affairs/Guangdong Vegetable Engineering and Technology Research Center, Guangdong Provincial Key Laboratory of Postharvest Science of Fruits and Vegetables, College of Horticulture, South China Agricultural University, Guangzhou 510642, China.
Hortic Res. 2023 Nov 27;11(1):uhad246. doi: 10.1093/hr/uhad246. eCollection 2024 Jan.
Bacterial wilt caused by is a severe soil-borne disease globally, limiting the production in Solanaceae plants. SmNAC negatively regulated eggplant resistance to Bacterial wilt (BW) though restraining salicylic acid (SA) biosynthesis. However, other mechanisms through which SmNAC regulates BW resistance remain unknown. Here, we identified an interaction factor, SmDDA1b, encoding a substrate receptor for E3 ubiquitin ligase, from the eggplant cDNA library using SmNAC as bait. expression was promoted by inoculation and exogenous SA treatment. The virus-induced gene silencing of the suppressed the BW resistance of eggplants; overexpression enhanced the BW resistance of tomato plants. SmDDA1b positively regulates BW resistance by inhibiting the spread of within plants. The SA content and the SA biosynthesis gene and signaling pathway genes decreased in the -silenced plants but increased in -overexpression plants. Moreover, SmDDB1 protein showed interaction with SmCUL4 and SmDDA1b and protein degradation experiments indicated that SmDDA1b reduced SmNAC protein levels through proteasome degradation. Furthermore, SmNAC could directly bind the promoter and repress its transcription. Thus, SmDDA1b is a novel regulator functioning in BW resistance of solanaceous crops via the SmNAC-mediated SA pathway. Those results also revealed a negative feedback loop between SmDDA1b and SmNAC controlling BW resistance.
由[病原菌名称未给出]引起的青枯病是一种严重的全球土传病害，限制了茄科植物的产量。SmNAC通过抑制水杨酸（SA）生物合成负向调节茄子对青枯病（BW）的抗性。然而，SmNAC调节BW抗性的其他机制仍不清楚。在这里，我们以SmNAC为诱饵，从茄子cDNA文库中鉴定出一个相互作用因子SmDDA1b，它编码一种E3泛素连接酶的底物受体。SmDDA1b的表达受病原菌接种和外源SA处理的促进。SmDDA1b的病毒诱导基因沉默降低了茄子对BW的抗性；SmDDA1b的过表达增强了番茄植株对BW的抗性。SmDDA1b通过抑制病原菌在植物体内的传播正向调节BW抗性。在SmDDA1b沉默的植株中SA含量以及SA生物合成基因和信号通路基因减少，但在SmDDA1b过表达的植株中增加。此外，SmDDB1蛋白与SmCUL4和SmDDA1b存在相互作用，蛋白质降解实验表明SmDDA1b通过蛋白酶体降解降低SmNAC蛋白水平。此外，SmNAC可以直接结合[基因名称未给出]启动子并抑制其转录。因此，SmDDA1b是通过SmNAC介导的SA途径在茄科作物BW抗性中发挥作用的一种新型调节因子。这些结果还揭示了SmDDA1b和SmNAC之间控制BW抗性的负反馈环。
