ABSTRACT
Nitrated fatty acids (NO2-FAs) are formed by the addition reaction of nitric oxide- and nitrite-derived nitrogen dioxide with unsaturated fatty acids. Nitrated fatty acids act as signaling molecules in mammals through the formation of covalent adducts with cellular thiols. The study of NO2-FAs in plant systems constitutes an interesting and emerging area. The presence of NO2-FA has been reported in olives, peas, rice and in Arabidopsis. To gain a better understanding of the role of NO2-FA on plant physiology, we analyzed the effects of exogenous application of nitro-oleic acid (NO2-OA) to tomato cell cultures. We found that NO2-OA induced reactive oxygen species (ROS) production in a dose-dependent manner via activation of NADPH oxidases, which requires calcium entry from the extracellular compartment and protein kinase activation, a mechanism that resembles the plant defense responses. NO2-OA-induced ROS production, expression of plant defense genes and led to cell death. The mechanism of action of NO2-OA involves a reduction in the glutathione cellular pool and covalently addition reactions with protein thiols and reduced glutathione. Altogether, these results indicate that NO2-OA triggers responses associated with plant defense, revealing its possible role as a signal molecule in biotic stress.
- •NO2
- nitrogen dioxide
- •NO
- nitric oxide
- FA
- fatty acid
- GSH
- reduced glutathione
- H2O2
- hydrogen peroxyde
- NO2-FA
- nitro fatty acids
- NO2-Ln
- nitro-linolenic acid
- NO2-OA
- nitro-oleic acid
- OA
- oleic acid
- ROS
- reactive oxygen species
Footnotes
One-sentence summary: Nitrated fatty acids act as signaling molecules in tomato cells inducing ROS, reducing glutathione cellular pool, reacting with protein thiols and free GSH and triggering plant defense responses.
Funding information: This work was supported by the UNMdP, Consejo Nacional de Investigaciones Científicas y Técnicas, CONICET: PIP 219 and CONICET-NIH (to AML), Agencia Nacional de Promoción Científica y Tecnológica, ANPCyT; PICT-Raices 2013-0800 (to AML), NIH GM125944 (to FJS) and AHA 17GRN33660955 (to FJS).