scholarly journals Pseudomonas syringae pv. actinidiae Effector HopAU1 Interacts with Calcium-Sensing Receptor to Activate Plant Immunity

2022 ◽  
Vol 23 (1) ◽  
pp. 508
Author(s):  
Jinlong Zhang ◽  
Mingxia Zhou ◽  
Wei Liu ◽  
Jiajun Nie ◽  
Lili Huang
Keyword(s):  
Cell Death ◽  
Pseudomonas Syringae ◽  
Plant Pathogen ◽  
Plant Immunity ◽  
Resistance Breeding ◽  
Plant Diseases ◽  
Calcium Sensing Receptor ◽  
Callose Deposition ◽  
Calcium Sensing ◽  
Plant Pathogen Interaction

Kiwifruit canker, caused by Pseudomonas syringae pv. actinidiae (Psa), is a destructive pathogen that globally threatens the kiwifruit industry. Understanding the molecular mechanism of plant-pathogen interaction can accelerate applying resistance breeding and controlling plant diseases. All known effectors secreted by pathogens play an important role in plant-pathogen interaction. However, the effectors in Psa and their function mechanism remain largely unclear. Here, we successfully identified a T3SS effector HopAU1 which had no virulence contribution to Psa, but could, however, induce cell death and activate a series of immune responses by agroinfiltration in Nicotiana benthamiana, including elevated transcripts of immune-related genes, accumulation of reactive oxygen species (ROS), and callose deposition. We found that HopAU1 interacted with a calcium sensing receptor in N. benthamiana (NbCaS) as well as its close homologue in kiwifruit (AcCaS). More importantly, silencing CaS by RNAi in N. benthamiana greatly attenuated HopAU1-triggered cell death, suggesting CaS is a crucial component for HopAU1 detection. Further researches showed that overexpression of NbCaS in N. benthamiana significantly enhanced plant resistance against Sclerotinia sclerotiorum and Phytophthora capsici, indicating that CaS serves as a promising resistance-related gene for disease resistance breeding. We concluded that HopAU1 is an immune elicitor that targets CaS to trigger plant immunity.

scholarly journals Pectobacterium carotovorum Elicits Plant Cell Death with DspE/F but the P. carotovorum DspE Does Not Suppress Callose or Induce Expression of Plant Genes Early in Plant–Microbe Interactions

2011 ◽  
Vol 24 (7) ◽  
pp. 773-786 ◽  
Author(s):  
Hye-Sook Kim ◽  
Phanit Thammarat ◽  
Steven A. Lommel ◽  
Clifford S. Hogan ◽  
Amy O. Charkowski
Keyword(s):  
Gene Expression ◽  
Cell Death ◽  
Pseudomonas Syringae ◽  
Plant Cell ◽  
Expression Profiles ◽  
Gene Expression Profiles ◽  
Secretion System ◽  
Broad Host Range ◽  
Pectobacterium Carotovorum ◽  
Callose Deposition

The broad-host-range bacterial soft rot pathogen Pectobacterium carotovorum causes a DspE/F-dependent plant cell death on Nicotiana benthamiana within 24 h postinoculation (hpi) followed by leaf maceration within 48 hpi. P. carotovorum strains with mutations in type III secretion system (T3SS) regulatory and structural genes, including the dspE/F operon, did not cause hypersensitive response (HR)-like cell death and or leaf maceration. A strain with a mutation in the type II secretion system caused HR-like plant cell death but no maceration. P. carotovorum was unable to impede callose deposition in N. benthamiana leaves, suggesting that P. carotovorum does not suppress this basal immunity function. Within 24 hpi, there was callose deposition along leaf veins and examination showed that the pathogen cells were localized along the veins. To further examine HR-like plant cell death induced by P. carotovorum, gene expression profiles in N. benthamiana leaves inoculated with wild-type and mutant P. carotovorum and Pseudomonas syringae strains were compared. The N. benthamiana gene expression profile of leaves infiltrated with Pectobacterium carotovorum was similar to leaves infiltrated with a Pseudomonas syringae T3SS mutant. These data support a model where Pectobacterium carotovorum uses the T3SS to induce plant cell death in order to promote leaf maceration rather than to suppress plant immunity.

scholarly journals Draft Genome Sequence of Pseudomonas syringae RAYR-BL, a Strain Isolated from Natural Accessions of Arabidopsis thaliana Plants

2022 ◽  
Author(s):  
Isabel Fuenzalida-Valdivia ◽  
Maria Victoria Gangas ◽  
Diego Zavala ◽  
Ariel Herrera-Vásquez ◽  
Fabrice Roux ◽  
...  
Keyword(s):  
Arabidopsis Thaliana ◽  
Pseudomonas Syringae ◽  
Genome Sequence ◽  
Plant Pathogen ◽  
Environmental Conditions ◽  
Draft Genome ◽  
Draft Genome Sequence ◽  
Content Type ◽  
Molecular Features ◽  
Plant Pathogen Interaction

Here, we report the genome sequence of the P. syringae strain RAYR-BL, isolated from natural accessions of Arabidopsis plants. The draft genome sequence consists of 5.85 Mbp assembled in 110 contigs. The study of P. syringae RAYR-BL is a valuable tool to investigate molecular features of plant-pathogen interaction under environmental conditions.

scholarly journals molecular link from PAMP perception to a MAPK cascade associated with tomato disease resistance

2012 ◽  
Author(s):  
Guido Sessa ◽  
Gregory B. Martin
Keyword(s):  
Cell Death ◽  
Disease Resistance ◽  
Immune Responses ◽  
Map Kinase ◽  
Pseudomonas Syringae ◽  
Molecular Mechanisms ◽  
Plant Immunity ◽  
Defense Responses ◽  
Research Activities ◽  
Mapk Cascades

The research problem: The detection of pathogen-associated molecular patterns (PAMPs) by plant pattern recognition receptors (PRRs) is a key mechanism by which plants activate an effective immune response against pathogen attack. MAPK cascades are important signaling components downstream of PRRs that transduce the PAMP signal to activate various defense responses. Preliminary experiments suggested that the receptor-like cytoplasmickinase (RLCK) Mai5 plays a positive role in pattern-triggered immunity (PTI) and interacts with the MAPKKK M3Kε. We thus hypothesized that Mai5, as other RLCKs, functions as a component PRR complexes and acts as a molecular link between PAMP perception and activation of MAPK cascades. Original goals: The central goal of this research was to investigate the molecular mechanisms by which Mai5 and M3Kε regulate plant immunity. Specific objectives were to: 1. Determine the spectrum of PAMPs whose perception is transmitted by M3Kε; 2. Identify plant proteins that act downstream of M3Kε to mediate PTI; 3. Investigate how and where Mai5 interacts with M3Kε in the plant cell; 4. Examine the mechanism by which Mai5 contributes to PTI. Changes in research directions: We did not find convincing evidence for the involvement of M3Kε in PTI signaling and substituted objectives 1 and 3 with research activities aimed at the analysis of transcriptomic profiles of tomato plants during the onset of plant immunity, isolation of the novel tomato PRR FLS3, and investigation of the involvement of the RLCKBSKs in PTI. Main achievements during this research program are in the following major areas: 1. Functional characterization of Mai5. The function of Mai5 in PTI signaling was demonstrated by testing the effect of silencing the Mai5 gene by virus-induced gene silencing (VIGS) experiments and in cell death assays. Domains of Mai5 that interact with MAPKKKs and subcellular localization of Mai5 were analyzed in detail. 2. Analysis of transcriptional profiles during the tomato immune responses to Pseudomonas syringae (Pombo et al., 2014). We identified tomato genes whose expression is induced specifically in PTI or in effector-triggered immunity (ETI). Thirty ETI-specific genes were examined by VIGS for their involvement in immunity and the MAPKKK EPK1, was found to be required for ETI. 3. Dissection of MAP kinase cascades downstream of M3Kε (Oh et al., 2013; Teper et al., 2015). We identified genes that encode positive (SGT and EDS1) and negative (WRKY1 and WRKY2) regulators of the ETI-associated cell death mediated by M3Kε. In addition, the MKK2 MAPKK, which acts downstream of M3Kε, was found to interact with the MPK3 MAPK and specific MPK3 amino acids involved interaction were identified and found to be required for induction of cell death. We also identified 5 type III effectors of the bacterial pathogen Xanthomonaseuvesicatoria that inhibited cell death induced by components of ETI-associated MAP kinase cascades. 4. Isolation of the tomato PRR FLS3 (Hind et al., submitted). FLS3, a novel PRR of the LRR-RLK family that specifically recognizes the flagellinepitope flgII-28 was isolated. FLS3 was shown to bind flgII-28, to require kinase activity for function, to act in concert with BAK1, and to enhance disease resistance to Pseudomonas syringae. 5. Functional analysis of RLCKs of the brassinosteroid signaling kinase (BSK) family.Arabidopsis and tomato BSKs were found to interact with PRRs. In addition, certain ArabidospsisBSK mutants were found to be impaired in PAMP-induced resistance to Pseudomonas syringae. Scientific and agricultural significance: Our research activities discovered and characterized new molecular components of signaling pathways mediating recognition of invading pathogens and activation of immune responses against them. Increased understanding of molecular mechanisms of immunity will allow them to be manipulated by both molecular breeding and genetic engineering to produce plants with enhanced natural defense against disease.

scholarly journals Cucumber Mildew Resistance Locus O Interacts with Calmodulin and Regulates Plant Cell Death Associated with Plant Immunity

2019 ◽  
Vol 20 (12) ◽  
pp. 2995 ◽  
Author(s):  
Guangchao Yu ◽  
Xiangyu Wang ◽  
Qiumin Chen ◽  
Na Cui ◽  
Yang Yu ◽  
...  
Keyword(s):  
Cell Death ◽  
Fluorescent Protein ◽  
Plant Immunity ◽  
Bimolecular Fluorescence Complementation ◽  
Marker Genes ◽  
Resistance Locus ◽  
Callose Deposition ◽  
Cucumis Sativus L ◽  
Hypersensitive Cell Death ◽  
Mildew Resistance

Pathogen-induced cell death is closely related to plant disease susceptibility and resistance. The cucumber (Cucumis sativus L.) mildew resistance locus O (CsMLO1) and calmodulin (CsCaM3) genes, as molecular components, are linked to nonhost resistance and hypersensitive cell death. In this study, we demonstrate that CsMLO1 interacts with CsCaM3 via yeast two-hybrid, firefly luciferase (LUC) complementation and bimolecular fluorescence complementation (BiFC) experiments. A subcellular localization analysis of green fluorescent protein (GFP) fusion reveals that CsCaM3 is transferred from the cytoplasm to the plasma membrane in Nicotiana benthamiana, and CsCaM3 green fluorescence is significantly attenuated via the coexpression of CsMLO1 and CsCaM3. CsMLO1 negatively regulates CsCaM3 expression in transiently transformed cucumbers, and hypersensitive cell death is disrupted by CsCaM3 and/or CsMLO1 expression under Corynespora cassiicola infection. Additionally, CsMLO1 silencing significantly enhances the expression of reactive oxygen species (ROS)-related genes (CsPO1, CsRbohD, and CsRbohF), defense marker genes (CsPR1 and CsPR3) and callose deposition-related gene (CsGSL) in infected cucumbers. These results suggest that the interaction of CsMLO1 with CsCaM3 may act as a cell death regulator associated with plant immunity and disease.

scholarly journals Jasmonic Acid at the Crossroads of Plant Immunity and Pseudomonas syringae Virulence

2020 ◽  
Vol 21 (20) ◽  
pp. 7482
Author(s):  
Aarti Gupta ◽  
Mamta Bhardwaj ◽  
Lam-Son Phan Tran
Keyword(s):  
Jasmonic Acid ◽  
Plant Defense ◽  
Pseudomonas Syringae ◽  
Regulatory Networks ◽  
Genetic Manipulation ◽  
Plant Immunity ◽  
Stomatal Closure ◽  
Defense Responses ◽  
Plant Defense Responses ◽  
Callose Deposition

Sensing of pathogen infection by plants elicits early signals that are transduced to affect defense mechanisms, such as effective blockage of pathogen entry by regulation of stomatal closure, cuticle, or callose deposition, change in water potential, and resource acquisition among many others. Pathogens, on the other hand, interfere with plant physiology and protein functioning to counteract plant defense responses. In plants, hormonal homeostasis and signaling are tightly regulated; thus, the phytohormones are qualified as a major group of signaling molecules controlling the most widely tinkered regulatory networks of defense and counter-defense strategies. Notably, the phytohormone jasmonic acid mediates plant defense responses to a wide array of pathogens. In this review, we present the synopsis on the jasmonic acid metabolism and signaling, and the regulatory roles of this hormone in plant defense against the hemibiotrophic bacterial pathogen Pseudomonas syringae. We also elaborate on how this pathogen releases virulence factors and effectors to gain control over plant jasmonic acid signaling to effectively cause disease. The findings discussed in this review may lead to ideas for the development of crop cultivars with enhanced disease resistance by genetic manipulation.

scholarly journals Arabidopsis spliceosome factor SmD3 modulates immunity to Pseudomonas syringae infection

2021 ◽  
Author(s):  
Anna Golisz ◽  
Michal Krzyszton ◽  
Monika Stepien ◽  
Jakub Dolata ◽  
Justyna Piotrowska ◽  
...  
Keyword(s):  
Pseudomonas Syringae ◽  
Plant Immunity ◽  
Mrna Splicing ◽  
Mrna Levels ◽  
Stomatal Development ◽  
Callose Deposition ◽  
Small Nuclear Ribonucleoprotein ◽  
Genome Wide ◽  
Nuclear Ribonucleoprotein

SmD3 is a core component of the small nuclear ribonucleoprotein (snRNP) that is essential for pre-mRNA splicing. The role of Arabidopsis SmD3 in plant immunity was assessed by testing sensitivity of smd3a and smd3b mutants to Pseudomonas syringae pv. tomato (Pst) DC3000 infection and its pathogenesis effectors flagellin (flg22), EF-Tu (elf18) and coronatine (COR). Both smd3 mutants exhibited enhanced susceptibility to Pst accompanied by marked changes in the expression of key pathogenesis markers. mRNA levels of these factors were also altered upon treatment with Pseudomonas effectors. We showed that SmD3-b dysfunction impairs mainly stomatal immunity as a result of defects in stomatal development. Our genome-wide transcriptome analysis of the smd3b-1 mutant infected with Pst revealed that lack of SmD3-b deregulates defense against Pst infection at the transcriptional and posttranscriptional levels including defects in splicing and an altered pattern of alternative splicing. Other changes in the smd3b-1 mutant involved enhanced elf18- and flg22-induced callose deposition, reduction of flg22-triggered production of early ROS and boost of secondary ROS caused by Pst infection. Together, our data indicate that SmD3 contributes to the plant immune response possibly via regulation of mRNA splicing of key pathogenesis factors.

scholarly journals Arabidopsis Spliceosome Factor SmD3 Modulates Immunity to Pseudomonas syringae Infection

2021 ◽  
Vol 12 ◽  
Author(s):  
Anna Golisz ◽  
Michal Krzyszton ◽  
Monika Stepien ◽  
Jakub Dolata ◽  
Justyna Piotrowska ◽  
...  
Keyword(s):  
Pseudomonas Syringae ◽  
Plant Immunity ◽  
Mrna Splicing ◽  
Mrna Levels ◽  
Stomatal Development ◽  
Response Factors ◽  
Callose Deposition ◽  
Small Nuclear Ribonucleoprotein ◽  
Genome Wide ◽  
Nuclear Ribonucleoprotein

SmD3 is a core component of the small nuclear ribonucleoprotein (snRNP) that is essential for pre-mRNA splicing. The role of Arabidopsis SmD3 in plant immunity was assessed by testing sensitivity of smd3a and smd3b mutants to Pseudomonas syringae pv. tomato (Pst) DC3000 infection and its pathogenesis effectors flagellin (flg22), EF-Tu (elf18) and coronatine (COR). Both smd3 mutants exhibited enhanced susceptibility to Pst accompanied by marked changes in the expression of key pathogenesis markers. mRNA levels of major biotic stress response factors were also altered upon treatment with Pseudomonas effectors. Our genome-wide transcriptome analysis of the smd3b-1 mutant infected with Pst, verified by northern and RT-qPCR, showed that lack of SmD3-b protein deregulates defense against Pst infection at the transcriptional and posttranscriptional levels including defects in splicing and an altered pattern of alternative splicing. Importantly, we show that SmD3-b dysfunction impairs mainly stomatal immunity as a result of defects in stomatal development. We propose that it is the malfunction of the stomata that is the primary cause of an altered mutant response to the pathogen. Other changes in the smd3b-1 mutant involved enhanced elf18- and flg22-induced callose deposition, reduction of flg22-triggered production of early ROS and boost of secondary ROS caused by Pst infection. Together, our data indicate that SmD3 contributes to the plant immune response possibly via regulation of mRNA splicing of key pathogenesis factors.

scholarly journals Diverse AvrPtoB Homologs from Several Pseudomonas syringae Pathovars Elicit Pto-Dependent Resistance and Have Similar Virulence Activities

2006 ◽  
Vol 72 (1) ◽  
pp. 702-712 ◽  
Author(s):  
Nai-Chun Lin ◽  
Robert B. Abramovitch ◽  
Young Jin Kim ◽  
Gregory B. Martin
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Pseudomonas Syringae ◽  
Plant Immunity ◽  
Amino Acid Identity ◽  
Host Genotype ◽  
New Genes ◽  
Pseudomonas Syringae Pathovars ◽  
Susceptible Tomato ◽  
Pto Kinase

ABSTRACT AvrPtoB is a type III effector protein from Pseudomonas syringae pv. tomato that physically interacts with the tomato Pto kinase and, depending on the host genotype, either elicits or suppresses programmed cell death associated with plant immunity. We reported previously that avrPtoB-related sequences are present in diverse gram-negative phytopathogenic bacteria. Here we describe characterization of avrPtoB homologs from P. syringae pv. tomato T1, PT23, and JL1065, P. syringae pv. syringae B728a, and P. syringae pv. maculicola ES4326. The avrPtoB homolog from P. syringae pv. maculicola, hopPmaL, was identified previously. The four new genes identified in this study are designated avrPtoBT1 , avrPtoBPT23 , avrPtoBJL1065 , and avrPtoBB728a . The AvrPtoB homologs exhibit 52 to 66% amino acid identity with AvrPtoB. Transcripts of each of the avrPtoB homologs were detected in the Pseudomonas strains from which they were isolated. Proteins encoded by the homologs were detected in all strains except P. syringae pv. tomato T1, suggesting that T1 suppresses accumulation of AvrPtoBT1. All of the homologs interacted with the Pto kinase in a yeast two-hybrid system and elicited a Pto-dependent defense response when they were delivered into leaf cells by DC3000ΔavrPtoΔavrPtoB, a P. syringae pv. tomato strain with a deletion of both avrPto and avrPtoB. Like AvrPtoB, all of the homologs enhanced the ability of DC3000ΔavrPtoΔavrPtoB to form lesions on leaves of two susceptible tomato lines. With the exception of HopPmaL which lacks the C-terminal domain, all AvrPtoB homologs suppressed programmed cell death elicited by the AvrPto-Pto interaction in an Agrobacterium-mediated transient assay. Thus, despite their divergent sequences, AvrPtoB homologs from diverse P. syringae pathovars have conserved avirulence and virulence activities similar to AvrPtoB activity.

Activating Antibodies to The Calcium-sensing Receptor in Immunotherapy-induced Hypoparathyroidism

2020 ◽  
Vol 105 (5) ◽  
pp. 1581-1588 ◽  
Author(s):  
Isabella Lupi ◽  
Alessandro Brancatella ◽  
Filomena Cetani ◽  
Francesco Latrofa ◽  
E Helen Kemp ◽  
...  
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
T Lymphocyte ◽  
Immune Checkpoint Inhibitors ◽  
Cytotoxic T Lymphocyte ◽  
Checkpoint Inhibitors ◽  
Calcium Sensing Receptor ◽  
Calcium Sensing ◽  
Cell Death Protein

Abstract Context Immune checkpoint inhibitors (ICIs), such as programmed cell death protein-1 (PD-1), programmed cell death protein-ligand 1 (PD-L1), and cytotoxic T lymphocyte antigen-4 (CTLA-4) monoclonal antibodies, are approved for the treatment of some types of advanced cancer. Their main treatment-related side-effects are immune-related adverse events (irAEs), especially thyroid dysfunction and hypophysitis. Hypoparathyroidism, on the contrary, is an extremely rare irAE. Objectives The aim of the study was to investigate the etiology of autoimmune hypoparathyroidism in a lung cancer patient treated with pembrolizumab, an anti-PD-1. Methods Calcium-sensing receptor (CaSR) autoantibodies, their functional activity, immunoglobulin (Ig) subclasses and epitopes involved in the pathogenesis of autoimmune hypoparathyroidism were tested. Results The patient developed hypocalcemia after 15 cycles of pembrolizumab. Calcium levels normalized with oral calcium carbonate and calcitriol and no remission of hypocalcemia was demonstrated during a 9-month follow-up. The patient was found to be positive for CaSR-stimulating antibodies, of IgG1 and IgG3 subclasses, that were able to recognize functional epitopes on the receptor, thus causing hypocalcemia. Conclusion The finding confirms that ICI therapy can trigger, among other endocrinopathies, hypoparathyroidism, which can be caused by pathogenic autoantibodies.

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