Rapid Induction of Distinct Stress Responses after the Release of Singlet Oxygen in Arabidopsis[W]
Author(s) -
Roel G.L. op den Camp,
Dominika Przybyla,
Christian Ochsenbein,
Christophe Laloi,
Chanhong Kim,
Antoine Da,
Daniela Wagner,
Éva Hideg,
Cornelia Göbel,
Ivo Feußner,
Meter,
Klaus Apel
Publication year - 2003
Publication title -
the plant cell
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.324
H-Index - 341
eISSN - 1532-298X
pISSN - 1040-4651
DOI - 10.1105/tpc.014662
Subject(s) - arabidopsis , reactive oxygen species , singlet oxygen , biology , superoxide , mutant , protochlorophyllide , biochemistry , biophysics , hydrogen peroxide , arabidopsis thaliana , photochemistry , intracellular , oxygen , microbiology and biotechnology , chloroplast , chemistry , gene , enzyme , organic chemistry
The conditional fluorescent (flu) mutant of Arabidopsis accumulates the photosensitizer protochlorophyllide in the dark. After a dark-to-light shift, the generation of singlet oxygen, a nonradical reactive oxygen species, starts within the first minute of illumination and was shown to be confined to plastids. Immediately after the shift, plants stopped growing and developed necrotic lesions. These early stress responses of the flu mutant do not seem to result merely from physicochemical damage. Peroxidation of chloroplast membrane lipids in these plants started rapidly and led to the transient and selective accumulation of a stereospecific and regiospecific isomer of hydroxyoctadecatrieonic acid, free (13S)-HOTE, that could be attributed almost exclusively to the enzymatic oxidation of linolenic acid. Within the first 15 min of reillumination, distinct sets of genes were activated that were different from those induced by superoxide/hydrogen peroxide. Collectively, these results demonstrate that singlet oxygen does not act primarily as a toxin but rather as a signal that activates several stress-response pathways. Its biological activity in Arabidopsis exhibits a high degree of specificity that seems to be derived from the chemical identity of this reactive oxygen species and/or the intracellular location at which it is generated.
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