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 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.

Managing Bacterial Speck and Spot of Tomato with Acibenzolar-S-Methyl in Virginia

2002 ◽  
Vol 3 (1) ◽  
pp. 11 ◽  
Author(s):  
A. S. Graves ◽  
S. A. Alexander
Keyword(s):  
Pseudomonas Syringae ◽  
Systemic Acquired Resistance ◽  
Block Design ◽  
Acquired Resistance ◽  
Copper Toxicity ◽  
Bacterial Disease ◽  
Tomato Production ◽  
Bacterial Speck ◽  
Run Off ◽  
Environmentally Sensitive Areas

On the Eastern Shore of Virginia, copper compounds, which have been used for controlling bacterial disease on tomato, have been associated with pesticide run-off from commercial tomato production with copper toxicity causing losses in clam nurseries. The objective of this study was to identify and evaluate a replacement for copper that was safer for the environment and could provide effective management of bacterial diseases of tomato. Acibenzolar-S-methyl (Actigard 50 WG), a plant activator that induces systemic acquired resistance (SAR), was compared to the standard bactericide (copper hydroxide + mancozeb) for controlling Xanthomonas axonopodis pv. vesicatoria and Pseudomonas syringae pv. tomato. Plots were established in grower fields in a randomized complete block design with four replications. Acibenzolar-S-methyl, at a rate of 10.5-g a.i./ha was equal to or better than the standard copper-based bactericide for controlling bacterial speck and spot, with no adverse affect on yield. Replacing copper with acibenzolar-S-methyl would effectively eliminate the need for copper bactericides. In environmentally sensitive areas where copper toxicity can be a problem, acibenzolar-S-methyl can providean effective alternative for the management of bacterial speck and bacterial spot on tomato. Accepted for publication 26 January 2002. Published 20 February 2002.

scholarly journals The NLR helper protein NRC3 but not NRC1 is required for Pto-mediated cell death in Nicotiana benthamiana

2015 ◽  
Author(s):  
Chih-Hang Wu ◽  
Khaoula Belhaj ◽  
Tolga O. Bozkurt ◽  
Sophien Kamoun
Keyword(s):  
Cell Death ◽  
Nicotiana Benthamiana ◽  
Rna Silencing ◽  
Genetic Complementation ◽  
Hypersensitive Cell Death ◽  
Immune Receptors ◽  
Disease Resistance Protein ◽  
Resistance Protein ◽  
Solanaceous Plants ◽  
Lrr Protein

Intracellular immune receptors of the nucleotide-binding leucine-rich repeat (NB-LRR or NLR) proteins often function in pairs, with "helper" proteins required for the activity of "sensors" that mediate pathogen recognition. The NLR helper NRC1 (NB-LRR protein required for HR-associated cell death 1) has been described as a signalling hub required for the cell death mediated by both cell surface and intracellular immune receptors in the model plant Nicotiana benthamiana. However, this work predates the availability of the N. benthamiana genome and whether NRC1 is indeed required for the reported phenotypes has not been confirmed. Here, we investigated the NRC family of solanaceous plants using a combination of genome annotation, phylogenetics, gene silencing and genetic complementation experiments. We discovered that a paralog of NRC1, we termed NRC3, is required for the hypersensitive cell death triggered by the disease resistance protein Pto but not Rx and Mi-1.2. NRC3 may also contribute to the hypersensitive cell death triggered by the receptor-like protein Cf-4. Our results highlight the importance of applying genetic complementation to validate gene function in RNA silencing experiments.

The small molecule Zaractin activates ZAR1-mediated immunity in Arabidopsis

2021 ◽  
Vol 118 (47) ◽  
pp. e2116570118
Author(s):  
Derek Seto ◽  
Madiha Khan ◽  
D. Patrick Bastedo ◽  
Alexandre Martel ◽  
Trinh Vo ◽  
...  
Keyword(s):  
Immune System ◽  
Pseudomonas Syringae ◽  
Small Molecule ◽  
Nucleotide Binding ◽  
Infection Process ◽  
Effector Proteins ◽  
Cellular Proteins ◽  
Leucine Rich Repeat ◽  
Effector Triggered Immunity ◽  
Immune Pathway

Pathogenic effector proteins use a variety of enzymatic activities to manipulate host cellular proteins and favor the infection process. However, these perturbations can be sensed by nucleotide-binding leucine-rich-repeat (NLR) proteins to activate effector-triggered immunity (ETI). Here we have identified a small molecule (Zaractin) that mimics the immune eliciting activity of the Pseudomonas syringae type III secreted effector (T3SE) HopF1r and show that both HopF1r and Zaractin activate the same NLR-mediated immune pathway in Arabidopsis. Our results demonstrate that the ETI-inducing action of pathogenic effectors can be harnessed to identify synthetic activators of the eukaryotic immune system.

scholarly journals Regulation of Tomato Prf by Pto-like Protein Kinases

2009 ◽  
Vol 22 (4) ◽  
pp. 391-401 ◽  
Author(s):  
Tatiana S. Mucyn ◽  
Ai-Jiuan Wu ◽  
Alexi L. Balmuth ◽  
Julia Maryam Arasteh ◽  
John P. Rathjen
Keyword(s):  
Protein Kinases ◽  
Pseudomonas Syringae ◽  
Kinase Activity ◽  
Negative Regulation ◽  
Effector Proteins ◽  
Leucine Rich Repeats ◽  
Direct Recognition ◽  
Fen Kinase ◽  
Bacterial Effectors ◽  
Pto Kinase

Tomato Prf encodes a nucleotide-binding domain shared by Apaf-1, certain R proteins, and CED-4 fused to C-terminal leucine-rich repeats (NBARC-LRR) protein that is required for bacterial immunity to Pseudomonas syringae and sensitivity to the organophosphate fenthion. The signaling pathways involve two highly related protein kinases. Pto kinase mediates direct recognition of the bacterial effector proteins AvrPto or AvrPtoB. Fen kinase is required for fenthion sensitivity and recognition of bacterial effectors related to AvrPtoB. The role of Pto and its association with Prf has been characterized but Fen is poorly described. We show that, similar to Pto, Fen requires N-myristoylation and kinase activity for signaling and interacts with the N-terminal domain of Prf. Thus, the mechanisms of activation of Prf by the respective protein kinases are similar. Prf–Fen interaction is underlined by coregulatory mechanisms in which Prf negatively regulates Fen, most likely by controlling kinase activity. We further characterized negative regulation of Prf by Pto, and show that regulation is mediated by the previously described negative regulatory patch. Remarkably, the effectors released negative regulation of Prf in a manner dependent on Pto kinase activity. The data suggest a model in which Prf associates generally with Pto-like kinases in tightly regulated complexes, which are activated by effector-mediated disruption of negative regulation. Release of negative regulation may be a general feature of activation of NBARC-LRR proteins by cognate effectors.

scholarly journals Pseudomonas Type III Effector AvrPto Suppresses the Programmed Cell Death Induced by Two Nonhost Pathogens in Nicotiana benthamiana and Tomato

2004 ◽  
Vol 17 (12) ◽  
pp. 1328-1336 ◽  
Author(s):  
Li Kang ◽  
Xiaoyan Tang ◽  
Kirankumar S. Mysore
Keyword(s):  
Cell Death ◽  
Disease Resistance ◽  
Programmed Cell Death ◽  
Pseudomonas Syringae ◽  
Type Iii Secretion ◽  
Nicotiana Benthamiana ◽  
Effector Proteins ◽  
Type Iii ◽  
Bacterial Pathogenicity ◽  
Suppression Effects

Many gram-negative bacterial pathogens rely on a type III secretion system to deliver a number of effector proteins into the host cell. Though a number of these effectors have been shown to contribute to bacterial pathogenicity, their functions remain elusive. Here we report that AvrPto, an effector known for its ability to interact with Pto and induce Pto-mediated disease resistance, inhibited the hypersensitive response (HR) induced by nonhost pathogen interactions. Pseudomonas syringae pv. tomato T1 causes an HR-like cell death on Nicotiana benthamiana. This rapid cell death was delayed significantly in plants inoculated with P. syringae pv. tomato expressing avrPto. In addition, P. syringae pv. tabaci expressing avrPto suppressed nonhost HR on tomato prf3 and ptoS lines. Transient expression of avrPto in both N. benthamiana and tomato prf3 plants also was able to suppress nonhost HR. Interestingly, AvrPto failed to suppress cell death caused by other elicitors and nonhost pathogens. AvrPto also failed to suppress cell death caused by certain gene-for-gene disease resistance interactions. Experiments with avrPto mutants revealed several residues important for the suppression effects. AvrPto mutants G2A, G99V, P146L, and a 12-amino-acid C-terminal deletion mutant partially lost the suppression ability, whereas S94P and I96T enhanced suppression of cell death in N. benthamiana. These results, together with other discoveries, demonstrated that suppression of host-programmed cell death may serve as one of the strategies bacterial pathoens use for successful invasion.

scholarly journals Receptors in the induction of the plant innate immunity

2021 ◽  
Author(s):  
Tian-Ying Yu ◽  
Meng-Kun Sun ◽  
Li-Kun Liang
Keyword(s):  
Immune Responses ◽  
Innate Immune System ◽  
Effector Proteins ◽  
Innate Immune ◽  
Leucine Rich Repeat ◽  
Nucleotide Binding Domain ◽  
Effector Triggered Immunity ◽  
Growth Development ◽  
Immune Pathway ◽  
Molecular Patterns

Plants adjust amplitude and duration of immune responses via different strategies to maintain growth, development and resistance to pathogens. Pathogen-associated molecular patterns (PAMPs)-triggered immunity (PTI) and effector-triggered immunity (ETI) play vital roles. PRRs (pattern recognition receptors), comprising a large number of receptor-like protein kinases (RLKs) and receptor-like proteins (RLPs), recognize related ligands and trigger immunity. PTI is the first layer of the innate immune system, and it recognizes PAMPs at plasma membrane to prevent infection. However, pathogens exploit effector proteins to bypass or directly inhibit the PTI immune pathway. Consistently, plants have evolved intracellular nucleotide-binding domain and leucine-rich repeat-containing (NLR) proteins to detect pathogenic effectors and trigger a hypersensitive response to activate ETI. PTI and ETI work together to protect plants from infection of virus and other pathogens. Diverse receptors and the corresponding ligands, especially several pairs of well-studied receptors and ligands in PTI immunity, are reviewed to illustrate the dynamic process of PTI response here.

Sign in / Sign up

Export Citation Format

Share Document