Estradiol-inducible AvrRps4 expression reveals distinct properties of TIR-NLR-mediated effector-triggered immunity

AbstractPlant nucleotide-binding domain, leucine-rich repeat receptor (NLR) proteins play important roles in recognition of pathogen-derived effectors. However, the mechanism by which plant NLRs activate immunity is still largely unknown. The paired Arabidopsis NLRs RRS1-R and RPS4, that confer recognition of bacterial effectors AvrRps4 and PopP2, are well studied, but how the RRS1/RPS4 complex activates early immediate downstream responses upon effector detection is still poorly understood. To study RRS1/RPS4 responses without the influence of cell-surface receptor immune pathways, we generated an Arabidopsis line with inducible expression of effector AvrRps4. Induction does not lead to hypersensitive cell death response (HR) but can induce electrolyte leakage, which often correlates with plant cell death. Activation of RRS1 and RPS4 without pathogens cannot activate mitogen-associated protein kinase cascades, but still activates upregulation of defense genes, and therefore resistance against bacteria.HighlightInducible expression of AvrRps4 activates RRS1/RPS4-mediated effector-triggered immunity without the presence of pathogens, allowing us to characterise downstream immune responses triggered by TIR-NLRs without cell-surface receptor-mediated immunity.

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Estradiol-inducible AvrRps4 expression reveals distinct properties of TIR-NLR-mediated effector-triggered immunity

Journal of Experimental Botany ◽

10.1093/jxb/erz571 ◽

2020 ◽

Vol 71 (6) ◽

pp. 2186-2197 ◽

Cited By ~ 8

Author(s):

Bruno Pok Man Ngou ◽

Hee-Kyung Ahn ◽

Pingtao Ding ◽

Amey Redkar ◽

Hannah Brown ◽

...

Keyword(s):

Cell Death ◽

Cell Surface Receptor ◽

Leucine Rich Repeat ◽

Nucleotide Binding Domain ◽

Hypersensitive Cell Death ◽

Cell Death Response ◽

Defence Genes ◽

Surface Receptor ◽

Effector Triggered Immunity ◽

Bacterial Effectors

Abstract Plant nucleotide-binding domain, leucine-rich repeat receptor (NLR) proteins play important roles in recognition of pathogen-derived effectors. However, the mechanism by which plant NLRs activate immunity is still largely unknown. The paired Arabidopsis NLRs RRS1-R and RPS4, that confer recognition of bacterial effectors AvrRps4 and PopP2, are well studied, but how the RRS1/RPS4 complex activates early immediate downstream responses upon effector detection is still poorly understood. To study RRS1/RPS4 responses without the influence of cell surface receptor immune pathways, we generated an Arabidopsis line with inducible expression of the effector AvrRps4. Induction does not lead to hypersensitive cell death response (HR) but can induce electrolyte leakage, which often correlates with plant cell death. Activation of RRS1 and RPS4 without pathogens cannot activate mitogen-associated protein kinase cascades, but still activates up-regulation of defence genes, and therefore resistance against bacteria.

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The helper NLR immune protein NRC3 mediates the hypersensitive cell death caused by the cell-surface receptor Cf-4

10.1101/2021.09.28.461843 ◽

2021 ◽

Author(s):

Jiorgos Kourelis ◽

Mauricio P. Contreras ◽

Adeline Harant ◽

Hiroaki Adachi ◽

Lida Derevnina ◽

...

Keyword(s):

Cell Death ◽

Cell Surface ◽

Immune Responses ◽

Coiled Coil ◽

Chimeric Protein ◽

Cell Surface Receptor ◽

Surface Pattern ◽

Hypersensitive Cell Death ◽

Cell Death Response ◽

Surface Receptor

Cell surface pattern recognition receptors (PRRs) activate immune responses that can include the hypersensitive cell death. However, the pathways that link PRRs to the cell death response are poorly understood. Here, we show that the cell surface receptor-like protein Cf-4 requires the intracellular nucleotide-binding domain leucine-rich repeat containing receptor (NLR) NRC3 to trigger a confluent cell death response upon detection of the fungal effector Avr4 in leaves of Nicotiana benthamiana. This NRC3 activity requires an intact N-terminal MADA motif, a conserved signature of coiled-coil (CC)-type plant NLRs that is required for resistosome-mediated immune responses. A chimeric protein with the N-terminal α1 helix of Arabidopsis ZAR1 swapped into NRC3 retains the capacity to mediate Cf-4 hypersensitive cell death. Pathogen effectors acting as suppressors of NRC3 can suppress Cf-4-triggered hypersensitive cell-death. Our findings link the NLR resistosome model to the hypersensitive cell death caused by a cell surface PRR.

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Mutual Potentiation of Plant Immunity by Cell-surface and Intracellular Receptors

10.1101/2020.04.10.034173 ◽

2020 ◽

Cited By ~ 9

Author(s):

Bruno Pok Man Ngou ◽

Hee-Kyung Ahn ◽

Pingtao Ding ◽

Jonathan DG Jones

Keyword(s):

Immune System ◽

Cell Surface ◽

Pseudomonas Syringae ◽

Plant Immunity ◽

Cell Surface Receptor ◽

Hypersensitive Cell Death ◽

Surface Receptors ◽

Intracellular Receptor ◽

Surface Receptor ◽

Immune Pathways

The plant immune system involves cell-surface receptors that detect intercellular pathogen-derived molecules, and intracellular receptors that activate immunity upon detection of pathogen-secreted effectors that act inside the plant cell. Surface receptor-mediated immunity has been extensively studied but in authentic interactions between plants and microbial pathogens, its presence impedes study of intracellular receptor-mediated immunity alone. How these two immune pathways interact is poorly understood. Here, we reveal mutual potentiation between these two recognition-dependent defense pathways. Recognition by surface receptors activates multiple protein kinases and NADPH oxidases, whereas intracellular receptors primarily elevate abundance of these proteins. Reciprocally, the intracellular receptor-dependent hypersensitive cell death response is strongly enhanced by activation of surface receptors. Activation of either immune system alone is insufficient to provide effective resistance against Pseudomonas syringae. Thus, immune pathways activated by cell-surface and intracellular receptors mutually potentiate to activate strong defense that thwarts pathogens. By studying the activation of intracellular receptors in the absence of surface receptor-mediated immunity, we have dissected the relationship between the two distinct immune systems. These findings reshape our understanding of plant immunity and have broad implications for crop improvement.

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