Constitutive activation of AtMEK5, a MAPK kinase, induces� salicylic acid-independent cell death in Arabidopsis thaliana

2004 ◽  
Vol 49 (24) ◽  
pp. 2594
Author(s):  
Hongxia LIU
Keyword(s):  
Arabidopsis Thaliana ◽  
Cell Death ◽  
Salicylic Acid ◽  
Mapk Kinase ◽  
Constitutive Activation

scholarly journals Arabidopsis thaliana cdd1 mutant uncouples the constitutive activation of salicylic acid signalling from growth defects

2011 ◽  
Vol 12 (9) ◽  
pp. 855-865 ◽  
Author(s):  
SWADHIN SWAIN ◽  
SHWETA ROY ◽  
JYOTI SHAH ◽  
SASKIA VAN WEES ◽  
CORNÉ M. PIETERSE ◽  
...  
Keyword(s):  
Arabidopsis Thaliana ◽  
Salicylic Acid ◽  
Constitutive Activation ◽  
Growth Defects

scholarly journals LSD1 Regulates Salicylic Acid Induction of Copper Zinc Superoxide Dismutase in Arabidopsis thaliana

1999 ◽  
Vol 12 (11) ◽  
pp. 1022-1026 ◽  
Author(s):  
Daniel J. Kliebenstein ◽  
Robert A. Dietrich ◽  
Adam C. Martin ◽  
Robert L. Last ◽  
Jeffery L. Dangl
Keyword(s):  
Arabidopsis Thaliana ◽  
Cell Death ◽  
Salicylic Acid ◽  
Pseudomonas Syringae ◽  
Lesion Formation ◽  
Copper Zinc Superoxide Dismutase ◽  
Zinc Superoxide Dismutase ◽  
A Cell ◽  
Copper Zinc ◽  
Cell Death Cascade

We characterized the accumulation patterns of Arabidopsis thaliana proteins, two CuZnSODs, FeSOD, MnSOD, PR1, PR5, and GST1, in response to various pathogen-associated treatments. These treatments included inoculation with virulent and avirulent Pseudomonas syringae strains, spontaneous lesion formation in the lsd1 mutant, and treatment with the salicylic acid (SA) analogs INA (2,6-dichloroisonicotinic acid) and BTH (benzothiadia-zole). The PR1, PR5, and GST1 proteins were inducible by all treatments tested, as expected from previous mRNA blot analysis. The two CuZnSOD proteins were induced by SA analogs and in conjunction with lsd1-mediated spreading cell death. Additionally, LSD1 is a part of a signaling pathway for the induction of the CuZnSOD proteins in response to SA but not in lsd1-mediated cell death. We suggest that the spreading lesion phenotype of lsd1 results from a lack of up-regulation of a CuZnSOD responsible for detoxification of accumulating superoxide before the reactive oxygen species can trigger a cell death cascade.

scholarly journals EDR2 negatively regulates salicylic acid-based defenses and cell death during powdery mildew infections of Arabidopsis thaliana

2007 ◽  
Vol 7 (1) ◽  
pp. 35 ◽  
Author(s):  
Sonja Vorwerk ◽  
Celine Schiff ◽  
Marjorie Santamaria ◽  
Serry Koh ◽  
Marc Nishimura ◽  
...  
Keyword(s):  
Arabidopsis Thaliana ◽  
Cell Death ◽  
Salicylic Acid ◽  
Powdery Mildew

scholarly journals Positive and Negative Regulation of Salicylic Acid-Dependent Cell Death and Pathogen Resistance in Arabidopsis lsd6 and ssi1 Mutants

2000 ◽  
Vol 13 (8) ◽  
pp. 877-881 ◽  
Author(s):  
Jean T. Greenberg
Keyword(s):  
Cell Death ◽  
Salicylic Acid ◽  
Genetic Basis ◽  
Higher Plants ◽  
Pathogen Resistance ◽  
Mechanisms Of Action ◽  
Negative Regulation ◽  
Positive Regulation ◽  
Constitutive Activation ◽  
Dependent Cell

Salicylic acid (SA) is a key defense molecule in higher plants that is required for resistance to diverse pathogens. A number of mutants of Arabidopsis with elevated resistance to pathogens and constitutive activation of defenserelated genes and cell death have been shown to require SA for all of their phenotypes. These mutants potentially identify interesting regulatory genes that control diverse SA responses. When dominant mutations confer SA-dependent phenotypes, it is important to know the genetic basis of dominance in order to draw conclusions on the possible mechanisms of action of the genes identified. Here I characterize the basis of the dominant phenotypes conferred by the ssi1 and lsd6 mutations. I show that ssi1 is haploinsufficient, while lsd6 is a gain-of-function mutation. Thus, SA-dependent responses are under both negative and positive regulation.

scholarly journals Salicylic Acid Accumulation Controlled by LSD1 Is Essential in Triggering Cell Death in Response to Abiotic Stress

Cells ◽  
2021 ◽  
Vol 10 (4) ◽  
pp. 962
Author(s):  
Maciej Jerzy Bernacki ◽  
Anna Rusaczonek ◽  
Weronika Czarnocka ◽  
Stanisław Karpiński
Keyword(s):  
Cell Death ◽  
Salicylic Acid ◽  
Abiotic Stress ◽  
Wild Type ◽  
Pr Genes ◽  
Genes Expression ◽  
Salicylic Acid Accumulation ◽  
Cell Death Phenotype ◽  
Insight Into

Salicylic acid (SA) is well known hormonal molecule involved in cell death regulation. In response to a broad range of environmental factors (e.g., high light, UV, pathogens attack), plants accumulate SA, which participates in cell death induction and spread in some foliar cells. LESION SIMULATING DISEASE 1 (LSD1) is one of the best-known cell death regulators in Arabidopsis thaliana. The lsd1 mutant, lacking functional LSD1 protein, accumulates SA and is conditionally susceptible to many biotic and abiotic stresses. In order to get more insight into the role of LSD1-dependent regulation of SA accumulation during cell death, we crossed the lsd1 with the sid2 mutant, caring mutation in ISOCHORISMATE SYNTHASE 1(ICS1) gene and having deregulated SA synthesis, and with plants expressing the bacterial nahG gene and thus decomposing SA to catechol. In response to UV A+B irradiation, the lsd1 mutant exhibited clear cell death phenotype, which was reversed in lsd1/sid2 and lsd1/NahG plants. The expression of PR-genes and the H2O2 content in UV-treated lsd1 were significantly higher when compared with the wild type. In contrast, lsd1/sid2 and lsd1/NahG plants demonstrated comparability with the wild-type level of PR-genes expression and H2O2. Our results demonstrate that SA accumulation is crucial for triggering cell death in lsd1, while the reduction of excessive SA accumulation may lead to a greater tolerance toward abiotic stress.

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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