Salicylic acid induces rapid inhibition of mitochondrial electron transport and oxidative phosphorylation in tobacco cells

Authors
Citation
Zx. Xie et Zx. Chen, Salicylic acid induces rapid inhibition of mitochondrial electron transport and oxidative phosphorylation in tobacco cells, PLANT PHYSL, 120(1), 1999, pp. 217-225
Citations number
53
Language
INGLESE
art.tipo
Article
Categorie Soggetti
Plant Sciences","Animal & Plant Sciences
Journal title
PLANT PHYSIOLOGY
ISSN journal
0032-0889 → ACNP
Volume
120
Issue
1
Year of publication
1999
Pages
217 - 225
Database
ISI
SICI code
0032-0889(199905)120:1<217:SAIRIO>2.0.ZU;2-A
Abstract
Salicylic acid (SA) is known to induce alternative pathway respiration by a ctivating 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 mu M induced inhibition of both ATP synthes is and respiratory O-2 uptake within minutes of incubation in tobacco (Nico tiana tabacum) cell cultures. Biologically active SA analogs capable of ind ucing pathogenesis-related genes and enhanced resistance also caused rapid inhibition of ATP synthesis and respiratory O-2 uptake, whereas biologicall y inactive analogs did not. Inhibition of ATP synthesis and respiratory O-2 uptake by SA was insensitive to the protein synthesis inhibitor cyclohexim ide, but was substantially reduced by the antioxidant N-acetylcysteine, sug gesting a possible role for reactive oxygen species in the inhibition of mi tochondrial functions. With exogenous NADH as the respiratory substrate, mi tochondria isolated from SA-treated tobacco cell cultures were found to hav e normal capacities for both ATP synthesis and respiratory O-2 uptake; dire ct incubation of isolated mitochondria with SA had no significant effect on these mitochondrial functions. These results indicate that (a) the respira tion capacities of isolated mitochondria do not correspond to the in vivo r espiration activities in SA-treated cell cultures and (b) the SA-induced in hibition of respiration in tobacco cell cultures may involve other componen ts that are not present in isolated mitochondria. Given the recently demons trated roles of mitochondria in plant disease resistance and animal apoptos is, this rapid inhibition by SA of mitochondrial functions may play a role in SA-mediated biological processes, including plant defense responses.