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Plasma membrane‐localized plant immune receptor targets H + ‐ATPase for membrane depolarization to regulate cell death
Author(s) -
Lee HyeYoung,
Seo YeEun,
Lee Joo Hyun,
Lee So Eui,
Oh Soohyun,
Kim Jihyun,
Jung Seungmee,
Kim Haeun,
Park Hyojeong,
Kim Sejun,
Mang Hyunggon,
Choi Doil
Publication year - 2022
Publication title -
new phytologist
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.742
H-Index - 244
eISSN - 1469-8137
pISSN - 0028-646X
DOI - 10.1111/nph.17789
Subject(s) - depolarization , membrane , microbiology and biotechnology , programmed cell death , receptor , biophysics , membrane potential , atpase , plant cell , biology , immune system , chemistry , biochemistry , apoptosis , enzyme , immunology , gene
Summary The hypersensitive response (HR) is a robust immune response mediated by nucleotide‐binding, leucine‐rich repeat receptors (NLRs). However, the early molecular event that links activated NLRs to cell death is unclear. Here, we demonstrate that NLRs target plasma membrane H + ‐ATPases (PMAs) that generate electrochemical potential, an essential component of living cells, across the plasma membrane. CC A 309, an autoactive N‐terminal domain of a coiled‐coil NLR (CNL) in pepper, is associated with PMAs. Silencing or overexpression of PMAs reversibly affects cell death induced by CC A 309 in Nicotiana benthamiana . CC A 309‐induced extracellular alkalization causes plasma membrane depolarization, followed by cell death. Coimmunoprecipitation analyses suggest that CC A 309 inhibits PMA activation by preoccupying the dephosphorylated penultimate threonine residue of PMA. Moreover, pharmacological experiments using fusicoccin, an irreversible PMA activator, showed that inhibition of PMAs contributes to CNL‐type (but not Toll interleukin‐1 receptor NLR‐type) resistance protein‐induced cell death. We suggest PMAs as primary targets of plasma membrane‐associated CNLs leading to HR‐associated cell death by disturbing the electrochemical gradient across the membrane. These results provide new insight into NLR‐mediated cell death in plants, as well as innate immunity in higher eukaryotes.