| Literature DB >> 31316205 |
Wang Tian1, Congcong Hou1, Zhijie Ren2, Chao Wang1, Fugeng Zhao3, Douglas Dahlbeck1, Songping Hu1, Liying Zhang2, Qi Niu2, Legong Li2, Brian J Staskawicz1, Sheng Luan4.
Abstract
Pathogen-associated molecular patterns (PAMPs) activate innate immunity in both animals and plants. Although calcium has long been recognized as an essential signal for PAMP-triggered immunity in plants, the mechanism of PAMP-induced calcium signalling remains unknown1,2. Here we report that calcium nutrient status is critical for calcium-dependent PAMP-triggered immunity in plants. When calcium supply is sufficient, two genes that encode cyclic nucleotide-gated channel (CNGC) proteins, CNGC2 and CNGC4, are essential for PAMP-induced calcium signalling in Arabidopsis3-7. In a reconstitution system, we find that the CNGC2 and CNGC4 proteins together-but neither alone-assemble into a functional calcium channel that is blocked by calmodulin in the resting state. Upon pathogen attack, the channel is phosphorylated and activated by the effector kinase BOTRYTIS-INDUCED KINASE1 (BIK1) of the pattern-recognition receptor complex, and this triggers an increase in the concentration of cytosolic calcium8-10. The CNGC-mediated calcium entry thus provides a critical link between the pattern-recognition receptor complex and calcium-dependent immunity programs in the PAMP-triggered immunity signalling pathway in plants.Entities:
Mesh：
Substances：
Year: 2019 PMID： 31316205 DOI： 10.1038/s41586-019-1413-y
Source DB: PubMed Journal: Nature ISSN： 0028-0836 Impact factor: 49.962