Arabidopsis EDS1 Connects Pathogen Effector Recognition to Cell Compartment–Specific Immune Responses

Abstract

Pathogen effectors are intercepted by plant intracellular nucleotide binding-leucine-rich repeat (NB-LRR) receptors. However, processes linking receptor activation to downstream defenses remain obscure. Nucleo-cytoplasmic basal resistance regulator EDS1 (ENHANCED DISEASE SUSCEPTIBILITY1) is indispensible for immunity mediated by TIR (Toll-interleukin-1 receptor)-NB-LRR receptors. We show that Arabidopsis EDS1 molecularly connects TIR-NB-LRR disease resistance protein RPS4 recognition of bacterial effector AvrRps4 to defense pathways. RPS4-EDS1 and AvrRps4-EDS1 complexes are detected inside nuclei of living tobacco cells after transient coexpression and in Arabidopsis soluble leaf extracts after resistance activation. Forced AvrRps4 localization to the host cytoplasm or nucleus reveals cell compartment-specific RPS4-EDS1 defense branches. Although nuclear processes restrict bacterial growth, programmed cell death and transcriptional resistance reinforcement require nucleo-cytoplasmic coordination. Thus, EDS1 behaves as an effector target and activated TIR-NB-LRR signal transducer for defenses across cell compartments.

The Coiled-Coil and Nucleotide Binding Domains of BROWN PLANTHOPPER RESISTANCE14 Function in Signaling and Resistance against Planthopper in Rice

“…Indeed, there is a growing body of evidence indicating that disease resistance and HR-related programmed cell death are distinct processes. Support for this hypothesis comes from studies on Rx (Slootweg et al, 2010), RPS4 (Heidrich et al, 2011), and N (Bhattacharjee et al, 2009). Moreover, cell death appears to be uncoupled from the defense mechanisms induced by plant disease resistance genes encoding R proteins such as Rdg2a (Bulgarelli et al, 2010), Rrs1 (Lehnackers and Knogge, 1990), Mla1 (Freialdenhoven et al, 1994), Rx (Bendahmane et al, 1999), RPS4, RPS6 (Gassmann, 2005), and Mi-1 (Martinez de Ilarduya et al, 2003).…”

“…This leads to the rapid appearance of necrotic lesions resulting from a process known as HR-like cell death, which occurs at the site of attempted pathogen invasion and is believed to limit the spread of biotrophic pathogens. However, the restriction of pathogen growth does not always correlate with cell death (Bendahmane et al, 1999;Gassmann, 2005;Coll et al, 2011;Heidrich et al, 2011). Although the transgenic plants were resistant to planthoppers, neither the isolated CC and NB domains nor the FL BPH14 protein induced hypersensitive cell death when expressed transiently in the authentic system (rice protoplasts) or an ectopic system (N. benthamiana leaves) (Figures 2A and 2D).…”

TIR-only protein RBA1 recognizes a pathogen effector to regulate cell death inArabidopsis

“…Pto DC3000 containing HopBA1 is still growth restricted on Col-0, indicating a decoupling of cell death and disease resistance. Decoupling of cell death and disease resistance has been previously reported (47)(48)(49). HopBA1 is not present naturally in Pto DC3000, so better understanding its contribution to disease resistance might require future studies in its endogenous strains (P. syringae pv.…”

TheArabidopsis thalianaTCP transcription factors: A broadening horizon beyond development

“…64 SRFR1 exists as an adaptor protein in cytoplasmic microsomal and nuclear protein complexes containing the defense regulator ENHANCED DISEASE SUSCEPTIBILITY1 (EDS1) and resistance proteins of the TIR-NB-LRR class. 106,107 The Arabidopsis accession RLD carrying the srfr1-1 allele exhibits enhanced resistance to DC3000 (avrRps4) but not to virulent DC30000, and excluding SRFR1 from the nucleus disables the complementation of the srfr1-1 mutant. 108 This observation suggests that a nuclear activity of SRFR is required for its function in suppressing resistance to DC30000 (avrRps4) in RLD plants.…”