The Arabidopsis aberrant growth and death2 mutant shows resistance to Pseudomonas syringae and reveals a role for NPR1 in suppressing hypersensitive cell death

2001 ◽  
Vol 27 (3) ◽  
pp. 203-211 ◽  
Author(s):  
Debra N. Rate ◽  
Jean T. Greenberg
Keyword(s):  
Cell Death ◽  
Pseudomonas Syringae ◽  
Hypersensitive Cell Death

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.

scholarly journals Nitric oxide Does Not Trigger Early Programmed Cell Death Events but May Contribute to Cell-to-Cell Signaling Governing Progression of the Arabidopsis Hypersensitive Response

2003 ◽  
Vol 16 (11) ◽  
pp. 962-972 ◽  
Author(s):  
Chu Zhang ◽  
Kirk J. Czymmek ◽  
Allan D. Shapiro
Keyword(s):  
Nitric Oxide ◽  
Cell Death ◽  
Pseudomonas Syringae ◽  
Hypersensitive Response ◽  
Plasma Membranes ◽  
No Production ◽  
Post Inoculation ◽  
Hypersensitive Cell Death ◽  
Synthase Inhibitor ◽  
Kinetics Of

Nitric oxide (NO) has been suggested to play a role in the hypersensitive response (HR). Single- and double-label fluorescence microscopy experiments were conducted using Arabidopsis leaves infected with Pseudomonas syringae pv. tomato DC3000 carrying either avrB or avrRpt2. Kinetics of NO production were followed by measurement of green 4-amino-5-methylamino-2′,7′-difluorofluorescein (DAF-FM) triazole fluorescence in leaves coinfiltrated with DAF-FM diacetate. Kinetics of hypersensitive cell death were followed by measurement of cytoplasmic red fluorescence following internalization of coinfiltrated propidium iodide through compromised plasma membranes. Neither NO accumulation nor cell death was seen until approximately 3 h postinoculation of Columbia leaves with DC3000·avrB or approximately 5.5 h post-inoculation with DC3000·avrRpt2. Subsequent NO accumulation kinetics closely paralleled HR progression in both Columbia and ndr1-1 mutant plants. These data established that NO accumulation does not happen sufficiently early for NO to be a signaling component controlling HR triggering. NO accumulation did contribute to the HR, as proven by an approximately 1-h delay in cell death kinetics caused by an NO scavenger or an NO synthase inhibitor. NO was first seen as punctate foci at the cell surface. Subsequent NO accumulation patterns were consistent with NO being an intercellular signal that functions in cell-to-cell spread of the HR.

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.

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 Uncoupling Salicylic Acid-Dependent Cell Death and Defense-Related Responses From Disease Resistance in the Arabidopsis Mutant acd5

Genetics ◽  
2000 ◽  
Vol 156 (1) ◽  
pp. 341-350
Author(s):  
Jean T Greenberg ◽  
F Paul Silverman ◽  
Hua Liang
Keyword(s):  
Cell Death ◽  
Salicylic Acid ◽  
Disease Resistance ◽  
Pseudomonas Syringae ◽  
Higher Plants ◽  
Ethylene Signaling ◽  
Symptom Development ◽  
Wild Type ◽  
Dependent Cell ◽  
Arabidopsis Mutant

Abstract Salicylic acid (SA) is required for resistance to many diseases in higher plants. SA-dependent cell death and defense-related responses have been correlated with disease resistance. The accelerated cell death 5 mutant of Arabidopsis provides additional genetic evidence that SA regulates cell death and defense-related responses. However, in acd5, these events are uncoupled from disease resistance. acd5 plants are more susceptible to Pseudomonas syringae early in development and show spontaneous SA accumulation, cell death, and defense-related markers later in development. In acd5 plants, cell death and defense-related responses are SA dependent but they do not confer disease resistance. Double mutants with acd5 and nonexpressor of PR1, in which SA signaling is partially blocked, show greatly attenuated cell death, indicating a role for NPR1 in controlling cell death. The hormone ethylene potentiates the effects of SA and is important for disease symptom development in Arabidopsis. Double mutants of acd5 and ethylene insensitive 2, in which ethylene signaling is blocked, show decreased cell death, supporting a role for ethylene in cell death control. We propose that acd5 plants mimic P. syringae-infected wild-type plants and that both SA and ethylene are normally involved in regulating cell death during some susceptible pathogen infections.

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