The putative effector BgtE-20069a, secreted from Blumeria graminis f. sp. tritici, suppresses plant immunity to facilitate wheat infection

文献类型： 外文期刊

第一作者： Yan, Tong

作者： Yan, Tong;Cheng, Gui;Zhai, Yamei;Wu, Lisha;Gong, Shuangjun;Yu, Dazhao;Yang, Lijun;Zeng, Fansong;Cheng, Gui;Zhai, Yamei;Wu, Lisha

作者机构：

关键词： Blumeria graminis f. sp. tritici; Effector; Virulence; Plant immunity

期刊名称：BMC MICROBIOLOGY （ 影响因子：4.2； 五年影响因子：4.8 ）

ISSN： 1471-2180

年卷期： 2025 年 25 卷 1 期

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收录情况： SCI

摘要： Cereal powdery mildews, which are caused by Blumeria graminis, are economically important diseases that are distributed throughout the world. To successfully evade the host defence mechanism, the wheat powdery mildew pathogen known as B. graminis f. sp. tritici (Bgt) 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 BgtE-20069a from Bgt. 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 Bgt infection in wheat. We observed that transient expression of BgtE-20069a in Nicotiana benthamiana suppressed programmed cell death (PCD) induced by both the proapoptotic protein Bax and the elicitor PAMP INF1 from Phytophthora infestans. 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 BgtE-20069a 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 Bgt infection in wheat; moreover, the results indicate that it can suppress plant immunity and increase Bgt virulence. Our findings broaden the current understanding of the role of effectors in promoting Bgt infection by manipulating host immunity, thereby providing new insights into the molecular mechanism of Bgt pathogenesis.

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