Premium
Changes in hydrogen peroxide homeostasis trigger an active cell death process in tobacco
Author(s) -
Dat James F.,
Pellinen Riikka,
Van De Cotte Brigitte,
Langebartels Christian,
Kangasjärvi Jaakko,
Inzé Dirk,
Van Breusegem Frank
Publication year - 2003
Publication title -
the plant journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.058
H-Index - 269
eISSN - 1365-313X
pISSN - 0960-7412
DOI - 10.1046/j.1365-313x.2003.01655.x
Subject(s) - hydrogen peroxide , homeostasis , microbiology and biotechnology , programmed cell death , chemistry , process (computing) , biology , biochemistry , apoptosis , computer science , operating system
Summary In transgenic tobacco plants with reduced catalase activity, high levels of hydrogen peroxide (H 2 O 2 ) can accumulate under photorespiratory conditions. Such a perturbation in H 2 O 2 homeostasis induced cell death in clusters of palisade parenchyma cells, primarily along the veins. Ultrastructural alterations, such as chromatin condensation and disruption of mitochondrial integrity, took place before cell death. Furthermore, enhanced transcript levels of mitochondrial defense genes accompanied these mitochondrial changes. Pharmacological data indicated that the initiation and execution of cell death require de novo protein synthesis and that the signal transduction pathway leading to cell death involved changes in ion homeostasis, (de)phosphorylation events and an oxidative burst, as observed during hypersensitive responses. This oxidase‐dependent oxidative burst is essential for cell death, but it is not required for the accumulation of defense proteins, suggesting a more prominent role for the oxidative burst in abiotic stress‐induced cell death.