scholarly journals Feedback Control of the Arabidopsis Hypersensitive Response

2004 ◽  
Vol 17 (4) ◽  
pp. 357-365 ◽  
Author(s):  
Chu Zhang ◽  
Annie Tang Gutsche ◽  
Allan D. Shapiro

The plant hypersensitive response (HR) to avirulent bacterial pathogens results from programmed cell death of plant cells in the infected region. Ion leakage and changes in signaling components associated with HR progression were measured. These studies compared Arabidopsis mutants affecting feedback loops with wild-type plants, with timepoints taken hourly. In response to Pseudomonas syringae pv. tomato DC3000·avrB, npr1-2 mutant plants showed increased ion leakage relative to wild-type plants. Hydrogen peroxide accumulation was similar to that in wild type, but salicylic acid accumulation was reduced at some timepoints. With DC3000·avrRpt2, similar trends were seen. In response to DC3000·avrB, ndr1-1 mutant plants showed more ion leakage than wild-type or npr1-2 plants. Hydrogen peroxide accumulation was delayed by approximately 1 h and reached half the level seen with wild-type plants. Salicylic acid accumulation was similar to npr1-2 mutant plants. With DC3000·avrRpt2, ndr1-1 mutant plants showed no ion leakage, no hydrogen peroxide accumulation, and minimal salicylic acid accumulation. Results with a ndr1-1 and npr1-2 double mutant were similar to ndr1-1. A model consistent with these data is presented, in which one positive and two negative regulatory circuits control HR progression. Understanding this circuitry will facilitate HR manipulation for enhanced disease resistance.

1991 ◽  
Vol 97 (4) ◽  
pp. 1342-1347 ◽  
Author(s):  
Jack B. Rasmussen ◽  
Raymond Hammerschmidt ◽  
Michael N. Zook

2012 ◽  
Vol 11 (6) ◽  
pp. 587-596 ◽  
Author(s):  
Xiao-yu Zheng ◽  
Natalie Weaver Spivey ◽  
Weiqing Zeng ◽  
Po-Pu Liu ◽  
Zheng Qing Fu ◽  
...  

1998 ◽  
Vol 11 (7) ◽  
pp. 702-705 ◽  
Author(s):  
Laurence Vallélian-Bindschedler ◽  
Jean-Pierre Métraux ◽  
Patrick Schweizer

Barley (Hordeum vulgare) seedlings were inoculated with the biotrophic pathogen Erysiphe graminis f. sp. hordei, the biotrophic nonhost pathogen E. graminis f. sp. tritici, and the necrotrophic nonhost pathogen Pseudomonas syringae pv. syringae. The levels of free salicylic acid and of salicylic-acid conjugates remained low after infection with E. graminis f. sp. hordei or E. graminis f. sp. tritici while they increased after inoculation with P. syringae pv. syringae. Pathogenesis-related proteins PR1, PR3 (chitinase), PR5 (thaumatin-like), and PR9 (peroxidase) accumulated after inoculation with all three pathogens.


Cells ◽  
2021 ◽  
Vol 10 (4) ◽  
pp. 962
Author(s):  
Maciej Jerzy Bernacki ◽  
Anna Rusaczonek ◽  
Weronika Czarnocka ◽  
Stanisław Karpiński

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.


Genetics ◽  
2000 ◽  
Vol 156 (1) ◽  
pp. 341-350
Author(s):  
Jean T Greenberg ◽  
F Paul Silverman ◽  
Hua Liang

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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