KEYNOTE PRESENTATION #2 LIVE AND LET DIE: A DEFENSE STRATEGY IN PLANTS
Xinnian Dong, Duke University
Yangnan Gu1, Shui Wang1,3, Sophie Zebell1, Zizhen Liang3, Byung-Ho Kang3 and Xinnian Dong1,*
1. Howard Hughes Medical Institute-Gordon and Betty Moore Foundation, Department of Biology, PO Box 90338, Duke University, Durham, North Carolina 27708, USA
2. Development Center of Plant Germplasm Resources, College of Life and Environmental Sciences, Shanghai Normal University, Shanghai 200234, China
3. School of Life Sciences, Centre for Cell and Developmental Biology and State Key Laboratory of Agrobiotechnology, The Chinese University of Hong Kong, Hong Kong, China
It has been a mystery how NB-LRR-mediated effector-triggered immunity (ETI) leads to PCD in plants in the absence of close homologs of caspases involved in pyroptosis during animal immune response-mediated by NLRs. Through a genetic screen for suppressors of a mutant with spontaneous PCD, cpr5, we found that the CKI-Rb-E2F cell cycle signaling pathway plays a key role in conferring PCD in plants during ETI mediated by both TIR-NB-LRR and CC-NB-LRR, two major classes of immune receptors in plants. Upon NB-LRR activation, CKIs are specifically released from association with the nuclear membrane protein CPR5, triggering E2F-mediated defense gene expression through hyperphosphorylation of Rb. Our recent work showed that CPR5 is a novel transmembrane nucleoporin. CPR5 associates with anchors of the NPC selective barrier to constrain nuclear access of signaling cargo and sequesters CKIs involved in ETI signal transduction. Upon activation by NB-LRRs, CPR5 undergoes an oligomer to monomer conformational switch, which coordinates CKI release for ETI signaling and reconfigures the selective barrier to allow significant influx of nuclear signaling cargo through the NPC. Consequently, these coordinated NPC actions result in simultaneous activation of diverse stress-related signaling pathways and constitute an essential regulatory mechanism specific for ETI/PCD induction.