scholarly journals A Bean cDNA Expressed During a Hypersensitive Reaction Encodes a Putative Calcium-Binding Protein

1999 ◽  
Vol 12 (8) ◽  
pp. 712-719 ◽  
Author(s):  
J. L. Jakobek ◽  
J. A. Smith-Becker ◽  
P. B. Lindgren
Keyword(s):  
Cell Death ◽  
Pseudomonas Syringae ◽  
Calcium Binding ◽  
Protein Product ◽  
Hypersensitive Reaction ◽  
Tobacco Necrosis Virus ◽  
Transcript Accumulation ◽  
Hypersensitive Cell Death ◽  
Binding Domains ◽  
Host Cell Death

The hypersensitive reaction (HR) is an inducible plant response that is associated with disease resistance. It is characterized by rapid, localized cell death at the site of infection and is believed to inhibit the spread of invading pathogens. We have isolated a cDNA clone, designated Hra32 (for hypersensitive reaction associated), corresponding to an RNA transcript that accumulates in bean during an HR. The predicted protein product of the Hra32 cDNA is an approximately 17 kDa protein of 161 amino acids, with four putative EF-hand calcium-binding domains. The temporal pattern of Hra32 transcript accumulation correlated closely with the onset of the HR in bean after inoculation with incompatible Pseudomonas syringae pv. tabaci and pv. tomato and with tobacco necrosis virus. Hra32 transcript also accumulated in bean in response to compatible P. syringae pv. phaseolicola and was correlated with necrotic cell death associated with disease lesion formation. A more transient pattern of Hra32 transcript accumulation occurred in bean in response to general stimuli that did not result in the HR or host cell death. These treatments included infiltration with a P. syringae pv. tabaci Hrp¯ mutant, P. syringae pv. tabaci cells treated with kanamycin, Escherichia coli, P. fluorescens, or glutathione, and in response to wounding. Thus, there was differential accumulation of the Hra32 transcript in response to specific stimuli resulting in the HR, compared with general stimuli that did not result in cell death. We hypothesize that the Hra32 product may be a component of the pathway that leads to hypersensitive cell death.

The Caenorhabditis elegans cell death gene ced-4 encodes a novel protein and is expressed during the period of extensive programmed cell death

Development ◽  
1992 ◽  
Vol 116 (2) ◽  
pp. 309-320 ◽  
Author(s):  
J. Yuan ◽  
H.R. Horvitz
Keyword(s):  
Cell Death ◽  
Caenorhabditis Elegans ◽  
Calcium Binding ◽  
Protein Product ◽  
Binding Domains ◽  
Cell Death Gene ◽  
Dna Fragment ◽  
Almost All ◽  
Rna Transcript ◽  
Novel Protein

Mutations in the gene ced-4 block almost all of the programmed cell deaths that normally occur during Caenorhabditis elegans development. We have cloned the ced-4 gene using a ced-4 mutation caused by the insertion of the transposon Tc4. When microinjected into a ced-4 animal, a 4.4 kb DNA fragment derived from the wild-type strain and corresponding to the region of the Tc4 insertion in the mutant ced-4(n1416) rescues the Ced-4 mutant phenotype. The ced-4 gene encodes a 2.2 kb RNA transcript. This mRNA is expressed primarily during embryogenesis, when most programmed cell deaths occur. The Ced-4 protein, as deduced from cDNA and genomic DNA clones, is 549 amino acids in length. Two regions of the putative Ced-4 protein product show some similarity to known calcium-binding domains.

scholarly journals Induction of Hypersensitive Cell Death by a Fungal Protein in Cultures of Tobacco Cells

1998 ◽  
Vol 11 (2) ◽  
pp. 115-123 ◽  
Author(s):  
Akira Yano ◽  
Kaoru Suzuki ◽  
Hirofumi Uchimiya ◽  
Hideaki Shinshi
Keyword(s):  
Cell Death ◽  
Specific Interaction ◽  
Trichoderma Viride ◽  
Defense Responses ◽  
Hypersensitive Reaction ◽  
Hypersensitive Cell Death ◽  
Tobacco Cells ◽  
Bright Yellow ◽  
Cell Death Program ◽  
Cellular Signal

Treatment of suspension-cultured tobacco (Nicotiana tabacum cv. Xanthi) cells (line XD6S) with fungal proteinaceous elicitors, namely, xylanase (EC 3.2.1.8) from Trichoderma viride (TvX) and xylanase from T. reesei (TrX), induced shrinkage of the cytoplasm, condensation of the nucleus, and, finally, cell death, which were accompanied by typical defense responses that included an oxidative burst and expression of defense genes. A Ca2+ channel blocker, Gd3+, inhibited the typical response of XD6S cells to TvX, which resembled the hypersensitive reaction (HR). These results suggested that the influx of Ca2+ ions plays an important role as a secondary signal. The HR was not observed in TvX-treated tobacco cells (line BY-2) derived from cv. Bright Yellow 2. This result suggests that key features of cultivar-specific interaction can be observed in cultures of tobacco cells. Xylanase from Bacillus circulans (BcX) and B. subtilis (BsX), which has enzymatic properties similar to those of TvX but an amino acid sequence different from that of TvX, did not induce the HR-like response in XD6S cells. These results suggest that the elicitor action of TvX is not due to its ability to hydrolyze cell walls but requires the TvX-specific recognition factors in plant cells. Thus, TvX-induced cell death was not due to some general toxic effect, but seems to be mediated by the activation of a specific cellular signal-transduction cascade that converges with a pathway that activates the intracellular cell death program.

scholarly journals A Salicylic Acid–Induced Lectin-Like Protein Plays a Positive Role in the Effector-Triggered Immunity Response of Arabidopsis thaliana to Pseudomonas syringae Avr-Rpm1

2013 ◽  
Vol 26 (12) ◽  
pp. 1395-1406 ◽  
Author(s):  
Grace Armijo ◽  
Paula Salinas ◽  
Mariela Inés Monteoliva ◽  
Aldo Seguel ◽  
Consuelo García ◽  
...  
Keyword(s):  
Cell Death ◽  
Salicylic Acid ◽  
Pseudomonas Syringae ◽  
Functional Characterization ◽  
Constitutive Expression ◽  
Hypersensitive Reaction ◽  
Positive Role ◽  
Legume Lectin ◽  
Immunity Response ◽  
Effector Triggered Immunity

Salicylic acid (SA) is one of the key hormones that orchestrate the pathogen-induced immune response in plants. This response is often characterized by the activation of a local hypersensitive reaction involving programmed cell death, which constrains proliferation of biotrophic pathogens. Here, we report the identification and functional characterization of an SA-induced legume lectin-like protein 1 (SAI-LLP1), which is coded by a gene that belongs to the group of early SA-activated Arabidopsis genes. SAI-LLP1 expression is induced upon inoculation with avirulent strains of Pseudomonas syringae pv. tomato via an SA-dependent mechanism. Constitutive expression of SAI-LLP1 restrains proliferation of P. syringae pv. tomato Avr-Rpm1 and triggers more cell death in inoculated leaves. Cellular and biochemical evidence indicates that SAI-LLP1 is a glycoprotein located primarily at the apoplastic side of the plasma membrane. This work indicates that SAI-LLP1 is involved in resistance to P. syringae pv. tomato Avr-Rpm1 in Arabidopsis, as a component of the SA-mediated defense processes associated with the effector-triggered immunity response.

scholarly journals XopQ induced stromule formation in Nicotiana benthamiana is causally linked to ETI signaling and depends on ADR1 and NRG1

2021 ◽  
Author(s):  
Jennifer Prautsch ◽  
Jessica L. Erickson ◽  
Sedef Özyürek ◽  
Rahel Gormannns ◽  
Lars Franke ◽  
...  
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Nicotiana Benthamiana ◽  
Double Mutant ◽  
Plant Immunity ◽  
Signaling Cascade ◽  
Nuclear Dynamics ◽  
Hypersensitive Cell Death ◽  
Host Cell Death ◽  
Dependent Cell

In Nicotiana benthamiana, expression of the Xanthomonas effector XopQ triggers ROQ1-dependent ETI responses and in parallel accumulation of plastids around the nucleus and the formation of stromules. Both processes were proposed to contribute to ETI-related hypersensitive cell death and thereby to plant immunity. Whether these reactions are directly connected to ETI signaling events has not been tested. Here we utilized transient expression experiments to determine whether XopQ-mediated plastid reactions are a result of XopQ perception by ROQ1 or a consequence of XopQ virulence activity. We find that N. benthamiana mutants lacking ROQ1, both RNLs (NRG1 and ADR1) or EDS1, fail to elicit XopQ-dependent host cell death and stromule formation. Mutants lacking only NRG1 lost XopQ-dependent cell death but retained some stromule induction that was abolished in the RNL double mutant. This analysis aligns XopQ-induced stromules with the ETI signaling cascade but not to host programmed cell death. Furthermore, data reveal that XopQ-triggered plastid clustering is not strictly linked to stromule formation during ETI. Our data suggest that stromule formation, in contrast to chloroplast peri-nuclear dynamics, is an integral part of the N. benthamiana ETI response and that both RNL sub-types play a role in this ETI response.

Infection-induced rapid cell death in plants: a means of efficient pathogen defense

1995 ◽  
Vol 73 (S1) ◽  
pp. 426-434 ◽  
Author(s):  
Elmon Schmelzer ◽  
Beatrix Naton ◽  
Sibylle Freytag ◽  
Ila Rouhara ◽  
Bernhard Küster ◽  
...  
Keyword(s):  
Cell Death ◽  
Defense Response ◽  
Pathogenic Bacteria ◽  
Cultured Cells ◽  
Defense Responses ◽  
Hypersensitive Reaction ◽  
Cellular Level ◽  
Comprehensive Description ◽  
Hypersensitive Cell Death ◽  
Transient Activation

The hypersensitive reaction represents one of the major means by which plants actively defend themselves against infection by pathogenic bacteria, fungi, viruses, and nematodes. This complex defense reaction, often associated with the synthesis of phytoalexins (antimicrobial secondary metabolites), involves at the cellular level highly dynamic cytoplasmic rearrangements, rapid metabolic changes, and finally cell death. It also correlates with the rapid and transient activation of various defense-related genes in a region of tissue surrounding infection sites and later, with the systemic increase in expression of a number of other genes. Examination of the reactions of individual living cells of potato leaves infected with Phytophthora infestans enabled the comprehensive description of the dynamic aspects of all stages of the defense response. Cytochemical investigations, employing cultured cells of parsley infected with P. infestans as a versatile model system, have contributed to a better understanding of cytoplasmic and metabolic processes occurring during the defense response, and suggest that hypersensitive cell death requires the preceding activation of respiration and specific metabolic pathways. Key words: defense responses, defense-related genes, hypersensitive reaction, programmed cell death.

scholarly journals Suppressors of the Arabidopsis lsd5 Cell Death Mutation Identify Genes Involved in Regulating Disease Resistance Responses

Genetics ◽  
1999 ◽  
Vol 151 (1) ◽  
pp. 305-319
Author(s):  
Jean-Benoit Morel ◽  
Jeffery L Dangl
Keyword(s):  
Cell Death ◽  
Disease Resistance ◽  
Pseudomonas Syringae ◽  
Plant Disease Resistance ◽  
Plant Disease ◽  
Disease Susceptibility ◽  
Bacterial Pathogen ◽  
Hypersensitive Reaction ◽  
Cell Death Phenotype ◽  
New Mutations

Abstract Cell death is associated with the development of the plant disease resistance hypersensitive reaction (HR). Arabidopsis lsd mutants that spontaneously exhibit cell death reminiscent of the HR were identified previously. To study further the regulatory context in which cell death acts during disease resistance, one of these mutants, lsd5, was used to isolate new mutations that suppress its cell death phenotype. Using a simple lethal screen, nine lsd5 cell death suppressors, designated phx (for the mythological bird Phoenix that rises from its ashes), were isolated. These mutants were characterized with respect to their response to a bacterial pathogen and oomycete parasite. The strongest suppressors—phx2, 3, 6, and 11-1—showed complex, differential patterns of disease resistance modifications. These suppressors attenuated disease resistance to avirulent isolates of the biotrophic Peronospora parasitica pathogen, but only phx2 and phx3 altered disease resistance to avirulent strains of Pseudomonas syringae pv tomato. Therefore, some of these phx mutants define common regulators of cell death and disease resistance. In addition, phx2 and phx3 exhibited enhanced disease susceptibility to different virulent pathogens, confirming probable links between the disease resistance and susceptibility pathways.

scholarly journals Cloning and Characterization of a Bean Udp-Glucosyltransferase cDNA Expressed During Plant-Bacterial Interactions

2001 ◽  
Vol 14 (1) ◽  
pp. 90-92 ◽  
Author(s):  
T. A. Sullivan ◽  
J. L. Jakobek ◽  
P. B. Lindgren
Keyword(s):  
Pseudomonas Syringae ◽  
Cdna Clone ◽  
Hypersensitive Reaction ◽  
Northern Analysis ◽  
Transcript Accumulation ◽  
Bacterial Interactions ◽  
Rna Transcript

A cDNA clone, which corresponds to an RNA transcript that accumulates in bean during the hypersensitive reaction, was isolated and designated Hra25 (for hypersensitive reaction associated). Hra25 is predicted to encode a UDP-glucosyltransferase. Northern analysis was used to study Hra25 transcript accumulation in bean in response to incompatible and compatible strains of Pseudomonas syringae, an Hrp¯ mutant, and wounding. Our data suggest that the Hra25 transcript is activated in response to specific avr-derived signals as well as non-avr, general signals.

scholarly journals Tissue Dependence and Differential Cordycepin Sensitivity of Race-Specific Resistance Responses in the Barley—Powdery Mildew Interaction

1997 ◽  
Vol 10 (7) ◽  
pp. 830-839 ◽  
Author(s):  
Ruth Schiffer ◽  
Regina Görg ◽  
Birgit Jarosch ◽  
Uli Beckhove ◽  
Gregor Bahrenberg ◽  
...  
Keyword(s):  
Cell Death ◽  
Powdery Mildew ◽  
Host Cell ◽  
Specific Resistance ◽  
Leaf Tissue ◽  
Primary Leaf ◽  
Hypersensitive Cell Death ◽  
Fungal Development ◽  
Interaction Sites ◽  
Host Cell Death

Epidermal cell monolayers prepared from partially dissected barley (Hordeum vulgare) coleoptiles were used for in vivo analysis of race-specific resistance to powdery mildew (Erysiphe graminis f. sp. hordei) specified by host genes Mla-1, Mla-12, and Mlg. Complete resistance governed by each of these genes is closely associated with hypersensitive cell death (hypersensitive response, HR) in primary leaf tissue. In contrast, Mla-12 coleoptile tissue reveals a fully compatible, Mla-1 coleoptile tissue a partially compatible, and Mlg coleoptile tissue an incompatible interaction upon challenge with pathogen races carrying corresponding avirulence functions. Quantitative recording of single plant-fungus interaction sites showed arrest of fungal development in papillae on Mlg coleoptiles. On Mla-1 and Mla-12 coleoptiles, attacked cells become predominantly penetrated by the fungus. Approximately one third of penetrated cells on Mla-1 coleoptiles subsequently undergo an HR. These sites reveal no further fungal development. Both Mlg and Mla-12 coleoptiles fail to mount an HR. The effect of cordycepin (3′-deoxyadenosine), an inhibitor of mRNA synthesis, was studied in planta on primary leaf tissue of Mla-12 and Mlg genotypes. Host cell death triggered by either gene is reduced to background levels observed in the near-isogenic compatible interaction and exhibits the same dose-dependent cordycepin sensitivity. Inhibition of Mlg-triggered, single-cell HR is not accompanied by release of fungal growth arrest, indicating cordycepin insensitivity of a papillae-associated resistance component. The data suggest that host cell death is a requisite component for expression of Mla-type but not Mlg-type resistance.

scholarly journals A Sec-Dependent Secretory Protein of the Huanglongbing-Associated Pathogen Suppresses Hypersensitive Cell Death in Nicotiana benthamiana

2020 ◽  
Vol 11 ◽  
Author(s):  
Chao Zhang ◽  
Peixiu Du ◽  
Hailin Yan ◽  
Zongcai Zhu ◽  
Xuefeng Wang ◽  
...  
Keyword(s):  
Gene Expression ◽  
Cell Death ◽  
Pseudomonas Syringae ◽  
Nicotiana Benthamiana ◽  
Transcriptome Profiling ◽  
Secretory Protein ◽  
Hypersensitive Cell Death ◽  
Challenge Inoculation ◽  
Transient Overexpression ◽  
Shock Proteins

“Candidatus Liberibacter asiaticus” (CLas) is a phloem-restricted Gram-negative bacterium that is the causal agent of citrus huanglongbing (HLB). In this study, we identified a CLas-encoded Sec-dependent secretory protein CLIBASIA_04405 that could contribute to the pathogenicity of this bacterium. The gene expression level of CLIBASIA_04405 was significantly higher in citrus than in psyllids. Transient overexpression of the mature CLIBASIA_04405 protein (m4405) in Nicotiana benthamiana leaves could suppress hypersensitive response (HR)-based cell death and H2O2 accumulation triggered by the mouse BAX and the Phytophthora infestans INF1. An alanine-substitution mutagenesis assay revealed the essential of amino acid clusters EKR45–47 and DE64–65 in cell death suppression. Challenge inoculation of the transgenic N. benthamiana-expressing m4405 with Pseudomonas syringae DC3000ΔhopQ1-1 demonstrated the greatly reduced bacterial proliferation. Remarkably, transcriptome profiling and RT-qPCR analysis disclosed that the gene expression of six small heat shock proteins (sHSPs), a set of plant defense regulators, were significantly elevated in the transgenic m4405 lines compared with those in wild-type N. benthamiana. In addition, the transgenic m4405 lines displayed phenotypes of dwarfism and leaf deformation. Altogether, these data indicated that m4405 was a virulence factor of CLas.

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