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A Coevolved EDS1-SAG101-NRG1 Module Mediates Cell Death Signaling by TIR-Domain Immune Receptors
Ist Teil von
The Plant cell, 2019-10, Vol.31 (10), p.2430-2455
Ort / Verlag
England: American Society of Plant Biologists
Erscheinungsjahr
2019
Link zum Volltext
Quelle
EZB Electronic Journals Library
Beschreibungen/Notizen
Plant nucleotide binding/leucine-rich repeat (NLR) immune receptors are activated by pathogen effectors to trigger host defenses and cell death. Toll-interleukin 1 receptor domain NLRs (TNLs) converge on the ENHANCED DISEASE SUSCEPTIBILITY1 (EDS1) family of lipase-like proteins for all resistance outputs. In Arabidopsis (
) TNL-mediated immunity,
EDS1 heterodimers with PHYTOALEXIN DEFICIENT4 (
PAD4) transcriptionally induced basal defenses.
EDS1 uses the same surface to interact with PAD4-related SENESCENCE-ASSOCIATED GENE101 (
SAG101), but the role of
EDS1-
SAG101 heterodimers remains unclear. We show that
EDS1-
SAG101 functions together with N REQUIRED GENE1 (
NRG1) coiled-coil domain helper NLRs as a coevolved TNL cell death-signaling module.
EDS1-
SAG101-
NRG1 cell death activity is transferable to the Solanaceous species
and cannot be substituted by
EDS1-
PAD4 with
NRG1 or
EDS1-
SAG101 with endogenous
NRG1. Analysis of EDS1-family evolutionary rate variation and heterodimer structure-guided phenotyping of
EDS1 variants and
PAD4-
SAG101 chimeras identify closely aligned ɑ-helical coil surfaces in the
EDS1-
SAG101 partner C-terminal domains that are necessary for reconstituted TNL cell death signaling. Our data suggest that TNL-triggered cell death and pathogen growth restriction are determined by distinctive features of EDS1-SAG101 and EDS1-PAD4 complexes and that these signaling machineries coevolved with other components within plant species or clades to regulate downstream pathways in TNL immunity.