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Function of endoplasmic reticulum calcium ATPase in innate immunity‐mediated programmed cell death
Author(s) -
Zhu Xiaohong,
Caplan Jeffrey,
Mamillapalli Padmavathi,
Czymmek Kirk,
DineshKumar Savithramma P
Publication year - 2010
Publication title -
the embo journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 7.484
H-Index - 392
eISSN - 1460-2075
pISSN - 0261-4189
DOI - 10.1038/emboj.2009.402
Subject(s) - biology , elicitor , microbiology and biotechnology , innate immune system , immune receptor , programmed cell death , endoplasmic reticulum , pattern recognition receptor , calcium atpase , immune system , calcium in biology , downregulation and upregulation , atpase , apoptosis , immunology , intracellular , biochemistry , enzyme , gene
Programmed cell death (PCD) initiated at the pathogen‐infected sites during the plant innate immune response is thought to prevent the development of disease. Here, we describe the identification and characterization of an ER‐localized type IIB Ca 2+ ‐ATPase (NbCA1) that function as a regulator of PCD. Silencing of NbCA1 accelerates viral immune receptor N‐ and fungal‐immune receptor Cf9‐mediated PCD, as well as non‐host pathogen Pseudomonas syringae pv. tomato DC3000 and the general elicitor cryptogein‐induced cell death. The accelerated PCD rescues loss‐of‐resistance phenotype of Rar1, HSP90‐silenced plants, but not SGT1‐silenced plants. Using a genetically encoded calcium sensor, we show that downregulation of NbCA1 results in the modulation of intracellular calcium signalling in response to cryptogein elicitor. We further show that NbCAM1 and NbrbohB function as downstream calcium decoders in N‐immune receptor‐mediated PCD. Our results indicate that ER‐Ca 2+ ‐ATPase is a component of the calcium efflux pathway that controls PCD during an innate immune response.