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Cell Host Microbe. 2014 Dec 10;16(6):787-94. doi: 10.1016/j.chom.2014.10.005. Epub 2014 Nov 20.

A noncanonical role for the CKI-RB-E2F cell-cycle signaling pathway in plant effector-triggered immunity.

Author information

1
Shanghai Center for Plant Stress Biology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai 201602, China; Department of Biology, Howard Hughes Medical Institute-Gordon and Betty Moore Foundation, P.O. Box 90338, Duke University, Durham, NC 27708, USA. Electronic address: swang@sibs.ac.cn.
2
Department of Biology, Howard Hughes Medical Institute-Gordon and Betty Moore Foundation, P.O. Box 90338, Duke University, Durham, NC 27708, USA.
3
Department of Biology, Howard Hughes Medical Institute-Gordon and Betty Moore Foundation, P.O. Box 90338, Duke University, Durham, NC 27708, USA. Electronic address: xdong@duke.edu.

Abstract

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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PMID:
25455564
PMCID:
PMC4282163
DOI:
10.1016/j.chom.2014.10.005
[Indexed for MEDLINE]
Free PMC Article
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