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Lysigenous aerenchyma formation in Arabidopsis thaliana in response to hypoxia is controlled by LESION SIMULATING DISEASE1
Stockholm University, Faculty of Science, Department of Botany.
2006 Article in journal (Refereed) Submitted
Place, publisher, year, edition, pages
URN: urn:nbn:se:su:diva-23034OAI: diva2:189946
Part of urn:nbn:se:su:diva-1358Available from: 2006-11-23 Created: 2006-11-23Bibliographically approved
In thesis
1. 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
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
Available from: 2006-11-23 Created: 2006-11-23 Last updated: 2013-12-10Bibliographically approved

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