Journal
CELL HOST & MICROBE
Volume 16, Issue 6, Pages 787-794Publisher
CELL PRESS
DOI: 10.1016/j.chom.2014.10.005
Keywords
-
Categories
Funding
- National Science Foundation [IOS-0744602, MCB-0519898]
- NIH [2R01-GM069594-09]
- Howard Hughes Medical Institute-Gordon and Betty Moore Foundation [GBMF3032]
- Chinese Academy of Sciences [XDB11030700]
- Environmental Protection Agency (EPA) [U915894]
- EPA [U915894, 1100201] Funding Source: Federal RePORTER
- Direct For Biological Sciences
- Division Of Integrative Organismal Systems [0929226] Funding Source: National Science Foundation
Ask authors/readers for more resources
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.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available