A mis-regulated cyclic nucleotide-gated channel mediates cytosolic calcium elevation and activates immunity in Arabidopsis
Autor: | Korbinian Schneeberger, Zichao Zheng, Yinhua Tang, Junli Wang, Jane E. Parker, Haitao Cui, Hequan Sun, Rong Su, Chunhui Zhao, Yanhong Zeng |
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Rok vydání: | 2020 |
Předmět: |
0106 biological sciences
0301 basic medicine Physiology Mutant Arabidopsis Cyclic Nucleotide-Gated Cation Channels Plant Science Protein Serine-Threonine Kinases 01 natural sciences 03 medical and health sciences Gene Expression Regulation Plant Plant Immunity Ion channel biology Chemistry Arabidopsis Proteins Calcium channel biology.organism_classification Cell biology Cytosol 030104 developmental biology Second messenger system Phosphorylation Calcium Nucleotides Cyclic Intracellular 010606 plant biology & botany |
Zdroj: | New Phytologist |
ISSN: | 1469-8137 |
Popis: | Calcium (Ca2+ ) is a second messenger for plant cell surface and intracellular receptors mediating pattern-triggered and effector-triggered immunity (respectively, PTI and ETI). Several CYCLIC NUCLEOTIDE-GATED CHANNELS (CNGCs) were shown to control transient cytosolic Ca2+ influx upon PTI activation. The contributions of specific CNGC members to PTI and ETI remain unclear. ENHANCED DISEASE SUSCEPTIBLITY1 (EDS1) regulates ETI signaling. In an Arabidopsis genetic screen for suppressors of eds1, we identify a recessive gain-of-function mutation in CNGC20, denoted cngc20-4, which partially restores disease resistance in eds1. cngc20-4 enhances PTI responses and ETI hypersensitive cell death. A cngc20-4 single mutant exhibits autoimmunity, which is dependent on genetically parallel EDS1 and salicylic acid (SA) pathways. CNGC20 self-associates, forms heteromeric complexes with CNGC19, and is phosphorylated and stabilized by BOTRYTIS INDUCED KINASE1 (BIK1). The cngc20-4 L371F exchange on a predicted transmembrane channel inward surface does not disrupt these interactions but leads to increased cytosolic Ca2+ accumulation, consistent with mis-regulation of CNGC20 Ca2+ -permeable channel activity. Our data show that ectopic Ca2+ influx caused by a mutant form of CNGC20 in cngc20-4 affects both PTI and ETI responses. We conclude that tight control of the CNGC20 Ca2+ ion channel is important for regulated immunity. |
Databáze: | OpenAIRE |
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