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

Journal Article (Journal Article)

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.

Full Text

Duke Authors

Cited Authors

  • Wang, S; Gu, Y; Zebell, SG; Anderson, LK; Wang, W; Mohan, R; Dong, X

Published Date

  • December 2014

Published In

Volume / Issue

  • 16 / 6

Start / End Page

  • 787 - 794

PubMed ID

  • 25455564

Pubmed Central ID

  • PMC4282163

Electronic International Standard Serial Number (EISSN)

  • 1934-6069

International Standard Serial Number (ISSN)

  • 1931-3128

Digital Object Identifier (DOI)

  • 10.1016/j.chom.2014.10.005


  • eng