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Potassium channel‐oxidative phosphorylation relationship in durum wheat mitochondria from control and hyperosmotic‐stressed seedlings
Author(s) -
TRONO DANIELA,
SOCCIO MARIO,
LAUS MAURA N.,
PASTORE DONATO
Publication year - 2011
Publication title -
plant, cell and environment
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.646
H-Index - 200
eISSN - 1365-3040
pISSN - 0140-7791
DOI - 10.1111/j.1365-3040.2011.02407.x
Subject(s) - oxidative phosphorylation , potassium , mitochondrion , potassium channel , phosphorylation , osmotic concentration , microbiology and biotechnology , chemistry , oxidative stress , biology , biophysics , biochemistry , organic chemistry
Durum wheat mitochondria (DWM) possess an ATP‐inhibited K + channel, the plant mitoK ATP (PmitoK ATP ), which is activated under environmental stress to control mitochondrial ROS production. To do this, PmitoK ATP collapses membrane potential (Δ Ψ ), thus suggesting mitochondrial uncoupling. We tested this point by studying oxidative phosphorylation (OXPHOS) in DWM purified from control seedlings and from seedlings subjected both to severe mannitol and NaCl stress. In severely‐stressed DWM, the ATP synthesis via OXPHOS, continuously monitored by a spectrophotometric assay, was about 90% inhibited when the PmitoK ATP was activated by KCl. Contrarily, in control DWM, although PmitoK ATP collapsed Δ Ψ , ATP synthesis, as well as coupling [respiratory control (RC) ratio and ratio between phosphorylated ADP and reduced oxygen (ADP/O)] checked by oxygen uptake experiments, were unaffected. We suggest that PmitoK ATP may play an important defensive role at the onset of the environmental/oxidative stress by preserving energy in a crucial moment for cell and mitochondrial bioenergetics. Consistently, under moderate mannitol stress, miming an early stress condition, the channel may efficiently control reactive oxygen species (ROS) generation (about 35‐fold from fully open to closed state) without impairing ATP synthesis. Anyway, if the stress significantly proceeds, the PmitoK ATP becomes fully activated by decrease of ATP concentration (25–40%) and increase of activators [free fatty acids (FFAs) and superoxide anion], thus impairing ATP synthesis.