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Light perception in plant disease defence signalling
Stockholm University, Faculty of Science, Department of Botany.
Stockholm University, Faculty of Science, Department of Botany.
Stockholm University, Faculty of Science, Department of Botany.
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2003 (English)In: Current opinion in plant biology, ISSN 1369-5266, E-ISSN 1879-0356, Vol. 6, no 4, 390-396 p.Article in journal (Refereed) Published
Abstract [en]

Light is a predominant factor in the control of plant growth, development and stress responses. Many biotic stress responses in plants are therefore specifically adjusted by the prevailing light conditions. The plant cell is equipped with sophisticated light-sensing mechanisms that are localised inside and outside of the chloroplast and the nucleus. Recent progress has provided models of how the signalling pathways that are involved in light perception and in defence could operate and interact to form a plant defence network. Such a signalling network includes systems to sense light and regulate gene expression. Photo-produced H2O2 and other reactive oxygen species in the cell also play an essential role in this regulatory network, controlling biotic and abiotic stress responses

Place, publisher, year, edition, pages
2003. Vol. 6, no 4, 390-396 p.
National Category
Botany
Identifiers
URN: urn:nbn:se:su:diva-24367DOI: 10.1016/S1369-5266(03)00061-XOAI: oai:DiVA.org:su-24367DiVA: diva2:197392
Note

Part of urn:nbn:se:su:diva-698

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
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Available from: 2005-10-20 Created: 2005-10-20 Last updated: 2014-10-02Bibliographically approved

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