Modulation of chloroplast components and defense responses during programmed cell death in tobacco infected with Pseudomonas syringae

2020 ◽  
Vol 528 (4) ◽  
pp. 753-759
Author(s):  
Bao Quoc Tran ◽  
Sunyo Jung
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Pseudomonas Syringae ◽  
Defense Responses

scholarly journals Harpin Inactivates Mitochondria in Arabidopsis Suspension Cells

2004 ◽  
Vol 17 (2) ◽  
pp. 131-139 ◽  
Author(s):  
Maren Krause ◽  
Jörg Durner
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Pseudomonas Syringae ◽  
Stress Responses ◽  
Time Course ◽  
Defense Responses ◽  
Ros Generation ◽  
Suspension Cells ◽  
Mitochondrial Functions ◽  
Arabidopsis Cells

Harpin is a well-known proteinaceous bacterial elicitor that can induce an oxidative burst and programmed cell death in various host plants. Given the demonstrated roles of mitochondria in animal apoptosis, we investigated the effect of harpin from Pseudomonas syringae on mitochondrial functions in Arabidopsis suspension cells in detail. Fluorescence microscopy in conjunction with double-staining for reactive oxygen species (ROS) and mitochondria suggested co-localization of mitochondria and ROS generation. Plant defense responses or cell death after pathogen attack have been suggested to be regulated by the concerted action of ROS and nitric oxide (NO). However, although Arabidopsis cells respond to harpin treatment with NO generation, time course analyses suggest that NO generation is not involved in initial responses but, rather, is a consequence of cellular decay. Among the fast responses we observed was a decrease of the mitochondrial membrane potential Δψm and, possibly as a direct consequence, of ATP production. Furthermore, treatment of Arabidopsis cells with harpin protein induced a rapid cytochrome C release from mitochondria into the cytosol, which is regarded as a hallmark of programmed cell death or apoptosis. Northern and DNA array analyses showed strong induction of protecting or scavenging systems such as alternative oxidase and small heat shock proteins, components that are known to be associated with cellular stress responses. In sum, the presented data suggest that harpin inactivates mitochondria in Arabidopsis cells.

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 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 Allelic Variants of the Pseudomonas syringae Type III Effector HopZ1 Are Differentially Recognized by Plant Resistance Systems

2009 ◽  
Vol 22 (2) ◽  
pp. 176-189 ◽  
Author(s):  
Huanbin Zhou ◽  
Robyn L. Morgan ◽  
David S. Guttman ◽  
Wenbo Ma
Keyword(s):  
Cell Death ◽  
Pseudomonas Syringae ◽  
Plant Resistance ◽  
Type Iii Secretion ◽  
Defense Responses ◽  
Plant Defense Responses ◽  
Type Iii Effectors ◽  
Type Iii ◽  
New Evidence ◽  
Bacterial Plant Pathogen

The bacterial plant pathogen Pseudomonas syringae depends on the type III secretion system and type III-secreted effectors to cause disease in plants. HopZ is a diverse family of type III effectors widely distributed in P. syringae isolates. Among the HopZ homologs, HopZ1 is ancient to P. syringae and has been shown to be under strong positive selection driven by plant resistance-imposed selective pressure. Here, we characterized the virulence and avirulence functions of the three HopZ1 alleles in soybean and Nicotiana benthamiana. In soybean, HopZ1 alleles have distinct functions: HopZ1a triggers defense response, HopZ1b promotes bacterial growth, and HopZ1c has no observable effect. In N. benthamiana, HopZ1a and HopZ1b both induce plant defense responses. However, they appear to trigger different resistance pathways, evidenced by two major differences between HopZ1a- and HopZ1b-triggered hypersensitive response (HR): i) the putative N-acylation sites had no effect on HopZ1a-triggered cell death, whereas it greatly enhanced HopZ1b-triggered cell death; and ii) the HopZ1b-triggered HR, but not the HopZ1a-triggered HR, was suppressed by another HopZ homolog, HopZ3. We previously demonstrated that HopZ1a most resembled the ancestral allelic form of HopZ1; therefore, this new evidence suggested that differentiated resistance systems have evolved in plant hosts to adapt to HopZ1 diversification in P. syringae.

scholarly journals A novel gene, phcA from Pseudomonas syringae induces programmed cell death in the filamentous fungus Neurospora crassa

2008 ◽  
Vol 68 (3) ◽  
pp. 672-689 ◽  
Author(s):  
Gale Wichmann ◽  
Jianping Sun ◽  
Karine Dementhon ◽  
N. Louise Glass ◽  
Steven E. Lindow
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Neurospora Crassa ◽  
Pseudomonas Syringae ◽  
Filamentous Fungus ◽  
Novel Gene

scholarly journals SPL36 Encodes a Receptor-like Protein Kinase that Regulates Programmed Cell Death and Defense Responses in Rice

Rice ◽  
2021 ◽  
Vol 14 (1) ◽  
Author(s):  
R. A. O. Yuchun ◽  
J. I. A. O. Ran ◽  
W. A. N. G. Sheng ◽  
W. U. Xianmei ◽  
Y. E. Hanfei ◽  
...  
Keyword(s):  
Cell Death ◽  
Salt Stress ◽  
Protein Kinase ◽  
Programmed Cell Death ◽  
Stress Responses ◽  
Defense Responses ◽  
Base Substitution ◽  
Wild Type ◽  
Salt Stress Response ◽  
Lesion Mimic

AbstractLesion mimic mutants spontaneously produce disease spots in the absence of biotic or abiotic stresses. Analyzing lesion mimic mutants’ sheds light on the mechanisms underlying programmed cell death and defense-related responses in plants. Here, we isolated and characterized the rice (Oryza sativa) spotted leaf 36 (spl36) mutant, which was identified from an ethyl methanesulfonate-mutagenized japonica cultivar Yundao population. spl36 displayed spontaneous cell death and enhanced resistance to rice bacterial pathogens. Gene expression analysis suggested that spl36 functions in the disease response by upregulating the expression of defense-related genes. Physiological and biochemical experiments indicated that more cell death occurred in spl36 than the wild type and that plant growth and development were affected in this mutant. We isolated SPL36 by map-based cloning. A single base substitution was detected in spl36, which results in a cysteine-to-arginine substitution in SPL36. SPL36 is predicted to encode a receptor-like protein kinase containing leucine-rich domains that may be involved in stress responses in rice. spl36 was more sensitive to salt stress than the wild type, suggesting that SPL36 also negatively regulates the salt-stress response. These findings suggest that SPL36 regulates the disease resistance response in rice by affecting the expression of defense- and stress-related genes.

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.

Red light delays programmed cell death in non-host interaction between Pseudomonas syringae pv tomato DC3000 and tobacco plants

Plant Science ◽  
2020 ◽  
Vol 291 ◽  
pp. 110361 ◽  
Author(s):  
Laura Moyano ◽  
María P. Lopéz-Fernández ◽  
Analía Carrau ◽  
Julián M. Nannini ◽  
Silvana Petrocelli ◽  
...  
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Pseudomonas Syringae ◽  
Red Light ◽  
Tomato Dc3000 ◽  
Tobacco Plants ◽  
Host Interaction

scholarly journals Engineering a Decoy Substrate in Soybean to Enable Recognition of the Soybean Mosaic Virus NIa Protease

2019 ◽  
Vol 32 (6) ◽  
pp. 760-769 ◽  
Author(s):  
Matthew Helm ◽  
Mingsheng Qi ◽  
Shayan Sarkar ◽  
Haiyue Yu ◽  
Steven A. Whitham ◽  
...  
Keyword(s):  
Cell Death ◽  
Mosaic Virus ◽  
Pseudomonas Syringae ◽  
Cleavage Site ◽  
Soybean Mosaic Virus ◽  
Defense Responses ◽  
Cell Death Response ◽  
Arabidopsis Protein ◽  
Systemic Spread ◽  
Nia Protease

In Arabidopsis, recognition of the AvrPphB effector protease from Pseudomonas syringae is mediated by the disease resistance (R) protein RPS5, which is activated by AvrPphB-induced cleavage of the Arabidopsis protein kinase PBS1. The recognition specificity of RPS5 can be altered by substituting the AvrPphB cleavage site within PBS1 with cleavage sequences for other proteases, including proteases from viruses. AvrPphB also activates defense responses in soybean (Glycine max), suggesting that soybean may contain an R protein analogous to RPS5. It was unknown, however, whether this response is mediated by cleavage of a soybean PBS1-like protein. Here, we show that soybean contains three PBS1 orthologs and that their products are cleaved by AvrPphB. Further, transient expression of soybean PBS1 derivatives containing a five-alanine insertion at their AvrPphB cleavage sites activated cell death in soybean protoplasts, demonstrating that soybean likely contains an AvrPphB-specific resistance protein that is activated by a conformational change in soybean PBS1 proteins. Significantly, we show that a soybean PBS1 decoy protein modified to contain a cleavage site for the soybean mosaic virus (SMV) NIa protease triggers cell death in soybean protoplasts when cleaved by this protease, indicating that the PBS1 decoy approach will work in soybean, using endogenous PBS1 genes. Lastly, we show that activation of the AvrPphB-dependent cell death response effectively inhibits systemic spread of SMV in soybean. These data also indicate that decoy engineering may be feasible in other crop plant species that recognize AvrPphB protease activity.

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