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Controlled levels of salicylic acid are required for optimal photosynthesis and redox homeostasis
Stockholm University, Faculty of Science, Department of Botany.
Stockholm University, Faculty of Science, Department of Botany.
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2006 (English)In: Journal of Experimental Botany, ISSN 0022-0957, E-ISSN 1460-2431, Vol. 57, no 8, 1795-1807 p.Article in journal (Refereed) Published
Abstract [en]

Sudden exposure of plants to high light (HL) leads to metabolic and physiological disruption of the photosynthetic cells. Changes in ROS content, adjustment of photosynthetic processes and the antioxidant pools and, ultimately, gene induction are essential components for a successful acclimation to the new light conditions. The influence of salicylic acid (SA) on plant growth, short-term acclimation to HL, and on the redox homeostasis of Arabidopsis thaliana leaves was assessed here. The dwarf phenotype displayed by mutants with high SA content (cpr1-1, cpr5-1, cpr6-1, and dnd1-1) was less pronounced when these plants were grown in HL, suggesting that the inhibitory effect of SA on growth was partly overcome at higher light intensities. Moreover, higher SA content affected energy conversion processes in low light, but did not impair short-term acclimation to HL. On the other hand, mutants with low foliar SA content (NahG and sid2-2) were impaired in acclimation to transient exposure to HL and thus predisposed to oxidative stress. Low and high SA levels were strictly correlated to a lower and higher foliar H2O2 content, respectively. Furthermore high SA was also associated with higher GSH contents, suggesting a tight correlation between SA, H2O2 and GSH contents in plants. These observations implied an essential role of SA in the acclimation processes and in regulating the redox homeostasis of the cell. Implications for the role of SA in pathogen defence signalling are also discussed.

Place, publisher, year, edition, pages
Oxford University Press, 2006. Vol. 57, no 8, 1795-1807 p.
Keyword [en]
Arabidopsis cross tolerance defence reactions glutathione hydrogen peroxide light acclimation photo-oxidative stress photosynthesis redox signalling salicylic acid
National Category
Botany
Identifiers
URN: urn:nbn:se:su:diva-24370DOI: 10.1093/jxb/erj196ISI: 000238768200020OAI: oai:DiVA.org:su-24370DiVA: diva2:197395
Available from: 2005-10-20 Created: 2005-10-20 Last updated: 2017-12-13Bibliographically approved
In thesis
1. Roles of LESIONS SIMULATING DISEASE1 and Salicylic Acid in Acclimation of Plants to Environmental Cues: Redox Homeostasis and physiological processes underlying plants responses to biotic and abiotic challenges
Open this publication in new window or tab >>Roles of LESIONS SIMULATING DISEASE1 and Salicylic Acid in Acclimation of Plants to Environmental Cues: Redox Homeostasis and physiological processes underlying plants responses to biotic and abiotic challenges
2005 (English)Doctoral thesis, comprehensive summary (Other academic)
Abstract [en]

In the natural environment plants are confronted to a multitude of biotic and abiotic stress factors that must be perceived, transduced, integrated and signaled in order to achieve a successful acclimation that will secure survival and reproduction. Plants have to deal with excess excitation energy (EEE) when the amount of absorbed light energy is exceeding that needed for photosynthetic CO2 assimilation. EEE results in ROS formation and can be enhanced in low light intensities by changes in other environmental factors.

The lesions simulating disease resistance (lsd1) mutant of Arabidopsis spontaneously initiates spreading lesions paralleled by ROS production in long day photoperiod and after application of salicylic acid (SA) and SA-analogues that trigger systemic acquired resistance (SAR). Moreover, the mutant fails to limit the boundaries of hypersensitive cell death (HR) after avirulent pathogen infection giving rise to the runaway cell death (rcd) phenotype. This ROS-dependent phenotype pointed towards a putative involvement of the ROS produced during photosynthesis in the initiation and spreading of the lesions.

We report here that the rcd has a ROS-concentration dependent phenotype and that the light-triggered rcd is depending on the redox-state of the PQ pool in the chloroplast. Moreover, the lower stomatal conductance and catalase activity in the mutant suggested LSD1 was required for optimal gas exchange and ROS scavenging during EEE. Through this regulation, LSD1 can influence the effectiveness of photorespiration in dissipating EEE. Moreover, low and high SA levels are strictly correlated to lower and higher foliar H2O2 content, respectively. This implies an essential role of SA in regulating the redox homeostasis of the cell and suggests that SA could trigger rcd in lsd1 by inducing H2O2 production.

LSD1 has been postulated to be a negative regulator of cell death acting as a ROS rheostat. Above a certain threshold, the pro-death pathway would operate leading to PCD. Our data suggest that LSD1 may be subjected to a turnover, enhanced in an oxidizing milieu and slowed down in a reducing environment that could reflect this ROS rheostat property. Finally, the two protein disulphide isomerase boxes (CGHC) present in the protein and the down regulation of the NADPH thioredoxin reductase (NTR) in the mutant connect the rcd to a putative impairment in the reduction of the cytosolic thioredoxin system. We propose that LSD1 suppresses the cell death processes through its control of the oxidation-reduction state of the TRX pool. An integrated model considers the role of LSD1 in both light acclimatory processes and in restricting pathogen-induced cell death.

Place, publisher, year, edition, pages
Stockholm: Botaniska institutionen, 2005. 46 p.
Keyword
LSD1, Photooxidative stress, Reactive oxygen species, Light acclimation, Photorespiration, Salicylic acid
National Category
Botany
Identifiers
urn:nbn:se:su:diva-698 (URN)91-7155-144-1 (ISBN)
Public defence
2005-11-11, föreläsningssalen, Botanicum, Lilla Frescativägen 5, Stockholm, 10:00
Opponent
Supervisors
Available from: 2005-10-20 Created: 2005-10-20 Last updated: 2014-10-02Bibliographically approved
2. Genetic and Molecular Mechanisms Controlling Reactive Oxygen Species and Hormonal Signalling of Cell Death in Response to Environmental Stresses in Arabidopsis thaliana
Open this publication in new window or tab >>Genetic and Molecular Mechanisms Controlling Reactive Oxygen Species and Hormonal Signalling of Cell Death in Response to Environmental Stresses in Arabidopsis thaliana
2006 (English)Doctoral thesis, comprehensive summary (Other academic)
Abstract [en]

In the present work the regulation of environmentally induced cell death and signaling of systemic acquired acclimation (SAA) in Arabidopsis thaliana is characterized. We used the lesion simulating disease1 (lsd1) mutant as a model system that is deregulated in light acclimation and programmed cell death (PCD). In this system we identify that redox status controlling SAA and cell death is controlled by the genes LSD1, EDS1, EIN2 and PAD4 which regulate cellular homeostasis of salicylic acid (SA), ethylene (ET), auxin (IAA) and reactive oxygen species (ROS). Furthermore we propose that the roles of LSD1 in light acclimation and in biotic stress are functionally linked. The influence of SA on plant growth, short-term acclimation to high light (HL), and on the redox homeostasis of Arabidopsis leaves was also assessed. SA impaired acclimation of wild-type plants to prolonged conditions of excess excitation energy (EEE). This indicates an essential role of SA in acclimation and regulation of cellular redox homeostasis. We also show that cell death in response to EEE is controlled by specific redox changes of photosynthetic electron transport carriers that normally regulate EEE acclimation. These redox changes cause production of ET that signals through the EIN2 gene and regulon. In the lsd1 mutant, we found that propagation of cell death depends on the plant defence regulators EDS1 and PAD4 operating upstream of ET production. We conclude that the balanced activities of LSD1, EDS1, PAD4 and EIN2 regulate chloroplast dependent acclimatory and defence responses. Furthermore, we show that Arabidopsis hypocotyls form lysigenous aerenchyma in response to hypoxia and that this process involves H2O2 and ET signalling. We found that formation of lysigenous aerenchyma depends on LSD1, EDS1 and PAD4. Conclusively we show that LSD1, EDS1 and PAD4, in their functions as major plant redox and hormone regulators provide a basis for fundamental plant survival in natural contitions.

Place, publisher, year, edition, pages
Stockholm: Botaniska institutionen, 2006. 50 p.
National Category
Botany
Identifiers
urn:nbn:se:su:diva-1358 (URN)91-7155-344-4 (ISBN)
Public defence
2006-12-14, föreläsningssalen, Botanicum, Lilla Frescativägen 5, Stockholm, 10:00
Opponent
Supervisors
Available from: 2006-11-23 Created: 2006-11-23 Last updated: 2013-12-10Bibliographically approved

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