Yan Tong, Cheng Gui, Zhai Yamei, Wu Lisha, Gong Shuangjun, Yu Dazhao, Yang Lijun, Zeng Fansong
Key Laboratory of Integrated Pest Management on Crops in Central China, Ministry of Agriculture and Rural Affairs, Hubei Key Laboratory of Crop Disease, Insect Pests and Weeds Control, Institute of Plant Protection and Soil Science, Hubei Academy of Agricultural Sciences, Wuhan, 430064, China.
College of Plant Science and Technology, Huazhong Agricultural University, Wuhan, 430070, China.
BMC Microbiol. 2025 Jul 2;25(1):389. doi: 10.1186/s12866-025-04110-4.
Cereal powdery mildews, which are caused by , are economically important diseases that are distributed throughout the world. To successfully evade the host defence mechanism, the wheat powdery mildew pathogen known as f. sp. () secretes an array of effectors into plant cells to interfere with host immunity and promote fungal invasion and colonisation during the infection process. However, little is known about the functions of the vast majority of these effectors in immune manipulation. In this study, we identified an effector-coding gene known as from . This gene encodes a short protein carrying an N-terminal signal peptide with a secretory function and is highly upregulated in the early stage of infection in wheat. We observed that transient expression of in suppressed programmed cell death (PCD) induced by both the proapoptotic protein Bax and the elicitor PAMP INF1 from The mature form of BgtE-20069a (which lacks a signal peptide) is localised to the cytoplasm and nucleus of plant cells. Moreover, the knockdown of resulted in reduced virulence towards wheat, with significantly decreased conidia production and a decreased haustorial formation rate being observed. Together, these results suggest that BgtE-20069a is a vital virulence factor that is required for infection in wheat; moreover, the results indicate that it can suppress plant immunity and increase virulence. Our findings broaden the current understanding of the role of effectors in promoting infection by manipulating host immunity, thereby providing new insights into the molecular mechanism of pathogenesis.
The online version contains supplementary material available at 10.1186/s12866-025-04110-4.
由[病原菌名称]引起的谷物白粉病是分布于世界各地的具有重要经济影响的病害。为了成功规避宿主防御机制，被称为[小麦白粉病菌学名]的小麦白粉病病原菌在感染过程中会向植物细胞分泌一系列效应子，以干扰宿主免疫并促进真菌的侵入和定殖。然而，对于这些效应子在免疫操纵中的绝大多数功能却知之甚少。在本研究中，我们从[病原菌名称]中鉴定出一个名为[效应子编码基因名称]的效应子编码基因。该基因编码一种携带具有分泌功能的N端信号肽的短蛋白，并且在小麦被[病原菌名称]感染的早期高度上调。我们观察到在[植物名称]中瞬时表达[效应子编码基因名称]可抑制由促凋亡蛋白Bax和来自[病原菌名称]的激发子PAMP INF1诱导的程序性细胞死亡（PCD）。BgtE - 20069a的成熟形式（缺少信号肽）定位于植物细胞的细胞质和细胞核。此外，敲低[效应子编码基因名称]导致对小麦的毒力降低，观察到分生孢子产量显著下降且吸器形成率降低。总之，这些结果表明BgtE - 20069a是小麦被[病原菌名称]感染所必需的重要毒力因子；此外，结果表明它可以抑制植物免疫并增加[病原菌名称]的毒力。我们的发现拓宽了目前对效应子通过操纵宿主免疫促进[病原菌名称]感染作用的理解，从而为[病原菌名称]致病的分子机制提供了新的见解。
在线版本包含可在10.1186/s12866 - 025 - 04110 - 4获取的补充材料。
