磷酸化
转录因子
细胞生物学
生物
基因沉默
重编程
调节器
植物抗病性
激酶
先天免疫系统
抄写(语言学)
WRKY蛋白质结构域
免疫
突变体
锌指
锌指转录因子
转录调控
系统获得性抵抗
信号转导
免疫系统
植物免疫
功能(生物学)
癌症研究
水杨酸
拟南芥
基因表达调控
突变
增强剂
化学
遗传学
转录因子Sp1
基因
RNA干扰
程序性细胞死亡
作者
Tingting Li,Yingying Liu,康雄 梶,Mengfan Li,Wenbin Wang,Yu Du
出处
期刊:Plant Journal
[Wiley]
日期:2026-04-01
卷期号:126 (2): e70873-e70873
被引量:1
摘要
Tomato production is severely threatened by late blight disease caused by Phytophthora infestans, yet durable control strategies remain limited. Identifying molecular resistance components is critical for sustainable disease management. Transcriptional reprogramming mediated by MAPK-regulated transcription factors (TFs) plays a pivotal role in plant immunity to Phytophthora and remains to be explored. Here, we identify the zinc finger-homeodomain transcription factor SlZHD7 as a positive regulator of tomato resistance to P. infestans. Functional analyses reveal that SlZHD7 induces salicylic acid-dependent plant cell death and enhances pathogen-associated molecular pattern (PAMP)-triggered immunity (PTI). Overexpression of SlZHD7 significantly enhances resistance, whereas its knockout compromises resistance. Furthermore, SlMPK4 interacts with and phosphorylates SlZHD7 at three threonine residues to stabilize it. Importantly, phosphorylation-deficient mutants fail to confer disease resistance, and MPK4 silencing abolishes SlZHD7-induced cell death, thereby establishing that MPK4-mediated phosphorylation is essential for the immune function of SlZHD7. Collectively, our study elucidates the function of the SlMPK4-SlZHD7 signaling module, demonstrating that MPK4-dependent phosphorylation stabilizes SlZHD7 to activate tomato resistance to P. infestans. These findings reveal mechanistic insights into late blight regulatory networks and highlight molecular targets for engineering crop resistance.
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