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

2020 ◽  
Vol 71 (6) ◽  
pp. 2186-2197 ◽  
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.

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

2019 ◽  
Author(s):  
Bruno Pok Man Ngou ◽  
Hee-Kyung Ahn ◽  
Pingtao Ding ◽  
Amey Redkar ◽  
Hannah Brown ◽  
...  
Keyword(s):  
Cell Death ◽  
Cell Surface ◽  
Inducible Expression ◽  
Cell Surface Receptor ◽  
Nucleotide Binding Domain ◽  
Hypersensitive Cell Death ◽  
Cell Death Response ◽  
Surface Receptor ◽  
Effector Triggered Immunity ◽  
Bacterial Effectors

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.

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

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.

scholarly journals Tomato Prf requires NLR helpers NRC2 and NRC3 to confer resistance against the bacterial speck pathogen Pseudomonas syringae pv. tomato

2019 ◽  
Author(s):  
Chih-Hang Wu ◽  
Sophien Kamoun
Keyword(s):  
Cell Death ◽  
Pseudomonas Syringae ◽  
Effector Proteins ◽  
Leucine Rich Repeat ◽  
Nucleotide Binding Domain ◽  
Hypersensitive Cell Death ◽  
Tomato Production ◽  
Bacterial Speck ◽  
Solanaceous Plants ◽  
Pto Kinase

AbstractBacterial speck, caused by the pathogen Pseudomonas syringae pv. tomato, is one of the most common diseases in tomato production. Together with Pto kinase, the NLR (nucleotide-binding domain leucine-rich repeat containing) protein Prf confers resistance against the bacterial speck pathogen by recognizing AvrPto and AvrPtoB, two Type III effector proteins secreted by P. syringae pv. tomato. This Prf/Pto pathway is part of a complex NLR network in solanaceous plants that mediates resistance to diverse pathogens through the helper NLR proteins NRCs (NLR required for cell death). We previously showed that, in Nicotiana benthamiana, the hypersensitive cell death elicited by expression of AvrPto and Pto, which activate immunity through the endogenous Prf ortholog NbPrf, requires functionally redundant NRC2 and NRC3. However, whether tomato (Solanum lycopersicum) Prf (SlPrf) confers resistance to the bacterial speck pathogen through NRC2 and NRC3 has not been determined. In this study, we show that SlPrf requires NRC2 and NRC3 to trigger hypersensitive cell death and disease resistance in both N. benthamiana and tomato. We found that the hypersensitive cell death induced by AvrPtoB/Pto/SlPrf in N. benthamiana is compromised when NRC2 and NRC3 are silenced, indicating that SlPrf is an NRC2/3-dependent NLR. We validated this finding by showing that silencing NRC2 and NRC3 in the bacterial speck resistant tomato ‘Rio Grande 76R’ compromised Prf-mediated resistance. These results indicate that the NRC network extends beyond N. benthamiana to solanaceous crops.

scholarly journals A chemical screen for suppressors of the avrRpm1-RPM1-dependent hypersensitive cell death response in Arabidopsis thaliana

Planta ◽  
2010 ◽  
Vol 231 (5) ◽  
pp. 1013-1023 ◽  
Author(s):  
Mario Serrano ◽  
David A. Hubert ◽  
Jeffery L. Dangl ◽  
Paul Schulze-Lefert ◽  
Erich Kombrink
Keyword(s):  
Arabidopsis Thaliana ◽  
Cell Death ◽  
Hypersensitive Cell Death ◽  
Cell Death Response ◽  
Chemical Screen

scholarly journals OsJAZ13 Negatively Regulates Jasmonate Signaling and Activates Hypersensitive Cell Death Response in Rice

2020 ◽  
Vol 21 (12) ◽  
pp. 4379
Author(s):  
Xiujing Feng ◽  
Lei Zhang ◽  
Xiaoli Wei ◽  
Yun Zhou ◽  
Yan Dai ◽  
...  
Keyword(s):  
Cell Death ◽  
Splice Variants ◽  
Adaptor Protein ◽  
Dependent Manner ◽  
Hypersensitive Cell Death ◽  
Cell Death Response ◽  
Jaz Proteins ◽  
Localization Analysis ◽  
And Function

Jasmonate ZIM-domain (JAZ) proteins belong to the subgroup of TIFY family and act as key regulators of jasmonate (JA) responses in plants. To date, only a few JAZ proteins have been characterized in rice. Here, we report the identification and function of rice OsJAZ13 gene. The gene encodes three different splice variants: OsJAZ13a, OsJAZ13b, and OsJAZ13c. The expression of OsJAZ13 was mainly activated in vegetative tissues and transiently responded to JA and ethylene. Subcellular localization analysis indicated OsJAZ13a is a nuclear protein. Yeast two-hybrid assays revealed OsJAZ13a directly interacts with OsMYC2, and also with OsCOI1, in a COR-dependent manner. Furthermore, OsJAZ13a recruited a general co-repressor OsTPL via an adaptor protein OsNINJA. Remarkably, overexpression of OsJAZ13a resulted in the attenuation of root by methyl JA. Furthermore, OsJAZ13a-overexpressing plants developed lesion mimics in the sheath after approximately 30–45 days of growth. Tillers with necrosis died a few days later. Gene-expression analysis suggested the role of OsJAZ13 in modulating the expression of JA/ethylene response-related genes to regulate growth and activate hypersensitive cell death. Taken together, these observations describe a novel regulatory mechanism in rice and provide the basis for elucidating the function of OsJAZ13 in signal transduction and cell death in plants.

scholarly journals Programmed Cell Death-1 Receptor (PD-1)-Mediated Regulation of Innate Lymphoid Cells

2019 ◽  
Vol 20 (11) ◽  
pp. 2836 ◽  
Author(s):  
Grace Mallett ◽  
Arian Laurence ◽  
Shoba Amarnath
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Innate Lymphoid Cells ◽  
Lymphoid Cells ◽  
Cell Surface Receptor ◽  
Programmed Cell Death 1 ◽  
Surface Receptor ◽  
A Cell ◽  
And Function

Programmed cell death-1 (PD-1) is a cell surface receptor that dampens adaptive immune responses. PD-1 is activated by the engagement of its ligands PDL-1 or PDL-2. This results in the inhibition of T cell proliferation, differentiation, cytokine secretion, and cytolytic function. Although a great deal is known about PD-1 mediated regulation of CD4+ and CD8+ T cells, its expression and function in innate lymphoid cells (ILCs) are yet to be fully deciphered. This review summarizes the role of PD-1 in (1) modulating ILC development, (2) ILC function, and (3) PD-1 signaling in ILC. Finally, we explore how PD-1 based immunotherapies may be beneficial in boosting ILC responses in cancer, infections, and other immune-related disorders.

scholarly journals The μ Subunit of Arabidopsis Adaptor Protein-2 Is Involved in Effector-Triggered Immunity Mediated by Membrane-Localized Resistance Proteins

2016 ◽  
Vol 29 (5) ◽  
pp. 345-351 ◽  
Author(s):  
Noriyuki Hatsugai ◽  
Rachel Hillmer ◽  
Shohei Yamaoka ◽  
Ikuko Hara-Nishimura ◽  
Fumiaki Katagiri
Keyword(s):  
Plasma Membrane ◽  
Immune Responses ◽  
Pseudomonas Syringae ◽  
Adaptor Protein ◽  
Floral Organ ◽  
Coated Vesicle ◽  
Defense Gene Expression ◽  
Hypersensitive Cell Death ◽  
Cell Death Response ◽  
Effector Triggered Immunity

Endocytosis has been suggested to be important in the cellular processes of plant immune responses. However, our understanding of its role during effector-triggered immunity (ETI) is still limited. We have previously shown that plant endocytosis, especially clathrin-coated vesicle formation at the plasma membrane, is mediated by the adaptor protein-2 (AP-2) complex and that loss of the μ subunit of AP-2 (AP2M) affects plant growth and floral organ development. Here, we report that AP2M is required for full-strength ETI mediated by the disease resistance (R) genes RPM1 and RPS2 in Arabidopsis. Reduced ETI was observed in an ap2m mutant plant, measured by growth of Pseudomonas syringae pv. tomato DC3000 strains carrying the corresponding effector genes avrRpm1 or avrRpt2 and by hypersensitive cell death response and defense gene expression triggered by these strains. In contrast, RPS4-mediated ETI and its associated immune responses were not affected by the ap2m mutation. While RPM1 and RPS2 are localized to the plasma membrane, RPS4 is localized to the cytoplasm and nucleus. Our results suggest that AP2M is involved in ETI mediated by plasma membrane–localized R proteins, possibly by mediating endocytosis of the immune receptor complex components from the plasma membrane.

Sign in / Sign up

Export Citation Format

Share Document