Concurrent activation of cell death‐regulating signaling pathways by singlet oxygen in Arabidopsis thaliana

Summary Upon a dark/light shift the conditional flu mutant of Arabidopsis starts to generate singlet oxygen (1O2), a non‐radical reactive oxygen species that is restricted to the plastid compartment. Immediately after the shift, plants stop growing and develop necrotic lesions. We have established a...

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Bibliographic Details
Published in:The Plant journal : for cell and molecular biology 2005-01, Vol.41 (1), p.68-80
Main Authors: Danon, Antoine, Miersch, Otto, Felix, Georg, Camp, Roel G.L., Apel, Klaus
Format: Article
Language:English
Subjects:
Arabidopsis - metabolism
Arabidopsis Proteins - genetics
Arabidopsis Proteins - metabolism
Arabidopsis thaliana
Biological and medical sciences
Cell Death
Cells
ethylene
Ethylenes - metabolism
Fundamental and applied biological sciences. Psychology
Fungi
Mutation
Oxygen
oxylipin
Plant physiology and development
Plant populations
programmed cell death
Protoplasts - metabolism
salicylic acid
Salicylic Acid - metabolism
Senescence and abscission
Signal Transduction
singlet oxygen
Singlet Oxygen - metabolism
Vegetative apparatus, growth and morphogenesis. Senescence
Vitamin B
Vitamin B 6 - metabolism
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Summary:Summary Upon a dark/light shift the conditional flu mutant of Arabidopsis starts to generate singlet oxygen (1O2), a non‐radical reactive oxygen species that is restricted to the plastid compartment. Immediately after the shift, plants stop growing and develop necrotic lesions. We have established a protoplast system, which allows detection and characterization of the death response in flu induced by the release of 1O2. Vitamin B6 that quenches 1O2 in fungi was able to protect flu protoplasts from cell death. Blocking ethylene production was sufficient to partially inhibit the death reaction. Similarly, flu mutant seedlings expressing transgenic NahG were partially protected from the death provoked by the release of 1O2, indicating a requirement for salicylic acid (SA) in this process, whereas in cells depleted of both, ethylene and SA, the extent of cell death was reduced to the wild‐type level. The flu mutant was also crossed with the jasmonic acid (JA)‐depleted mutant opr3, and with the JA, OPDA and dinor OPDA (dnOPDA)‐depleted dde2‐2 mutant. Analysis of the resulting double mutants revealed that in contrast to the JA‐induced suppression of H2O2/superoxide‐dependent cell death reported earlier, JA promotes singlet oxygen‐mediated cell death in flu, whereas other oxylipins such as OPDA and dnOPDA antagonize this death‐inducing activity of JA.
ISSN:0960-7412
1365-313X
DOI:10.1111/j.1365-313X.2004.02276.x