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Salicylic Acid Induces Rapid Inhibition of Mitochondrial Electron
Transport and Oxidative Phosphorylation
in Tobacco
Cells1
Zhixin Xie and
Zhixiang Chen*
Department of Microbiology, Molecular Biology and Biochemistry,
University of Idaho, Moscow, Idaho 83844-3052
Salicylic acid (SA) is known to
induce alternative pathway respiration by activating expression of the
alternative oxidase gene. In the present study we report a rapid mode
of action by SA on plant mitochondrial functions. SA at concentrations
as low as 20 µM induced inhibition of both ATP synthesis
and respiratory O2 uptake within minutes of incubation in
tobacco (Nicotiana tabacum) cell cultures. Biologically
active SA analogs capable of inducing pathogenesis-related genes and
enhanced resistance also caused rapid inhibition of ATP synthesis and
respiratory O2 uptake, whereas biologically inactive
analogs did not. Inhibition of ATP synthesis and respiratory
O2 uptake by SA was insensitive to the protein synthesis
inhibitor cycloheximide, but was substantially reduced by the
antioxidant N-acetylcysteine, suggesting a possible role for reactive oxygen species in the inhibition of mitochondrial functions. With exogenous NADH as the respiratory substrate,
mitochondria isolated from SA-treated tobacco cell cultures were found
to have normal capacities for both ATP synthesis and respiratory
O2 uptake; direct incubation of isolated mitochondria with
SA had no significant effect on these mitochondrial functions. These
results indicate that (a) the respiration capacities of isolated
mitochondria do not correspond to the in vivo respiration activities in
SA-treated cell cultures and (b) the SA-induced inhibition of
respiration in tobacco cell cultures may involve other components that
are not present in isolated mitochondria. Given the recently
demonstrated roles of mitochondria in plant disease resistance and
animal apoptosis, this rapid inhibition by SA of mitochondrial
functions may play a role in SA-mediated biological processes,
including plant defense responses.
1
This work was supported in part by Idaho
Agricultural Experimental Station and U.S. Department of Agriculture
grant no. 96-36301-3316 to Z.C. Z.X. was supported by a Plant
Biotechnology Graduate Assistantship from the University of Idaho
Institute for Molecular and Agricultural Genetic Engineering.
*
Corresponding author; e-mail zchen{at}uidaho.edu; fax
1-208-885-6518.
Plant Physiol. (1999) 120: 217-226
Copyright Clearance Center: 0032-0889/99/120//10
© 1999 American Society of Plant Physiologists
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