A noncanonical role for the CKI-RB-E2F cell-cycle signaling pathway in plant effector-triggered immunity.
A noncanonical role for the CKI-RB-E2F cell-cycle signaling pathway in plant effector-triggered immunity.
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DOI：
10.1016/j.chom.2014.10.005
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发表时间：
2014-12-10
影响因子：
30.3
通讯作者：
Dong X
中科院分区：
文献类型：
--
作者：
Wang S;Gu Y;Zebell SG;Anderson LK;Wang W;Mohan R;Dong X
植物免疫是植物主要的宿主防御机制，其机制往往与细胞程序性死亡（PCD）有关。植物缺乏半胱天冬酶的同源物，半胱天冬酶是动物PCD的关键介质。因此，尽管参与ETI的NB-LRR受体已被充分研究，但它们如何激活PCD并赋予抗病性仍然是难以捉摸的。我们发现，拟南芥核膜蛋白，CPR 5，负调控ETI和相关的PCD通过物理相互作用与细胞色素依赖性激酶抑制剂（CKIs）。在ETI诱导后，从CPR 5释放CKI以引起另一个核心细胞周期调节因子E2 F的过度激活。在cki和e2 f突变体中，由TIR-NB-LRR和CC-NB-LRR类免疫受体诱导的ETI应答受到损害。我们进一步表明，E2 F在ETI期间可能通过CKI介导的视网膜母细胞瘤相关蛋白1（RBR 1）过度磷酸化而失调。这项研究表明，经典的细胞周期调节因子也发挥重要的非经典作用，在植物免疫。
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 over-activation 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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