A mis-regulated cyclic nucleotide-gated channel mediates cytosolic calcium elevation and activates immunity in Arabidopsis

© 2021 The Authors New Phytologist © 2021 New Phytologist Foundation.

Bibliographische Detailangaben
Veröffentlicht in:The New phytologist. - 1979. - 230(2021), 3 vom: 19. Mai, Seite 1078-1094
1. Verfasser: Zhao, Chunhui (VerfasserIn)
Weitere Verfasser: Tang, Yinhua, Wang, Junli, Zeng, Yanhong, Sun, Hequan, Zheng, Zichao, Su, Rong, Schneeberger, Korbinian, Parker, Jane E, Cui, Haitao
Format: Online-Aufsatz
Sprache:English
Veröffentlicht: 2021
Zugriff auf das übergeordnete Werk:The New phytologist
Schlagworte:Journal Article Research Support, Non-U.S. Gov't CNGC EDS1 (ENHANCED DISEASE SUSCEPTIBLITY1) ETI (effector-triggered immunity) PTI calcium channel plant immunity Arabidopsis Proteins Cyclic Nucleotide-Gated Cation Channels mehr... Nucleotides, Cyclic BIK1 protein, Arabidopsis EC 2.7.11.1 Protein Serine-Threonine Kinases Calcium SY7Q814VUP
Beschreibung
Zusammenfassung:© 2021 The Authors New Phytologist © 2021 New Phytologist Foundation.
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
Beschreibung:Date Completed 14.05.2021
Date Revised 04.12.2021
published: Print-Electronic
Citation Status MEDLINE
ISSN:1469-8137
DOI:10.1111/nph.17218