生物
效应器
细胞生物学
E2F型
高磷酸化
视网膜母细胞瘤蛋白
细胞周期
调节器
免疫
信号转导
程序性细胞死亡
泛素
激酶
细胞
免疫系统
免疫学
遗传学
细胞凋亡
基因
作者
Shui Wang,Yangnan Gu,Sophia G. Zebell,Lisa Anderson,Wei Wang,Rajinikanth Mohan,Xinnian Dong
标识
DOI:10.1016/j.chom.2014.10.005
摘要
Summary
Effector-triggered immunity (ETI), the major host defense mechanism in plants, is often associated with programmed cell death (PCD). Plants lack close homologs of caspases, the key mediators of PCD in animals. So although the NB-LRR receptors involved in ETI are well studied, how they activate PCD and confer disease resistance remains elusive. We show that the Arabidopsis nuclear envelope protein, CPR5, negatively regulates ETI and the associated PCD through a physical interaction with cyclin-dependent kinase inhibitors (CKIs). Upon ETI induction, CKIs are released from CPR5 to cause overactivation of another core cell-cycle regulator, E2F. In cki and e2f mutants, ETI responses induced by both TIR-NB-LRR and CC-NB-LRR classes of immune receptors are compromised. We further show that E2F is deregulated during ETI, probably through CKI-mediated hyperphosphorylation of retinoblastoma-related 1 (RBR1). This study demonstrates that canonical cell-cycle regulators also play important noncanonical roles in plant immunity.
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