A pectin methylesterase inhibitor NtPMEI21 negatively regulates resistance to brown spot disease in Nicotiana tabacum L

文献类型： 外文期刊

第一作者： Bai, Yalin

作者： Bai, Yalin;Ji, Yan;Jiang, Zipeng;Liu, Zhengwen;Zhang, Yu;Jiang, Caihong;Yang, Aiguo;Cheng, Lirui;Liu, Dan;Li, Zunqiang;Zhang, Qiang

作者机构：

关键词： Pectin methylesterification; Pectin methylesterase inhibitor; Brown spot disease; Plant immunity

期刊名称：PLANT SCIENCE （ 影响因子：4.1； 五年影响因子：5.1 ）

ISSN： 0168-9452

年卷期： 2025 年 359 卷

页码：

收录情况： SCI

摘要： Pectin, as one of the major components of plant cell walls, plays a crucial role in cell wall integrity (CWI) which is closely linked with plant immunity. Pectin methylesterase (PME) catalyzes the demethylesterification of pectin and is modulated by the pectin methylesterase inhibitors (PMEIs). Here, we explored the expression patterns and the specific roles of NtPMEI21 on regulating the resistance to Alternaria alternata in tobacco (Nicotiana tabacum L.). By analyzing its protein sequence, we demonstrated that NtPMEI21 possessed a conserved PMEI domain. NtPMEI21 has a high expression level in leaves and is stimulated upon A. alternata infection. The NtPMEI21 protein is localized in the cell wall. The leaves of NtPMEI21 knockout line exhibited a lower degree of pectin methylesterification (DM) and an increase in resistance to fungal pathogen attacks with respect to the control plants. Furthermore, the expression of immunity-related marker genes, including NtWAK2 (pattern recognition receptor), NtGST (maintaining ROS homeostasis), NtCAL12 (callose synthase), and NtPDF1.2 (jasmonic acid signaling component) were markedly up-regulated in NtPMEI21 knockout line compared to control and NtPMEI21 overexpression lines. Our findings suggest NtPMEI21 as a negative regulator of cell wall-mediated resistance to brown spot disease, likely through WAK-mediated immune signaling pathway. Key message: NtPMEI21 was strongly induced in response to brown spot disease caused by Alternaria alternata in tobacco. NtPMEI21 negatively regulates cell wall-mediated resistance by affecting pectin methylesterification status and immunity-related gene expression.

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