Abstract
Nitric oxide (NO) regulates plant growth and development as well as responses to stress that enhanced its endogenous production. Arabidopsis plants exposed to a pulse of exogenous NO gas were used for untargeted global metabolomic analyses thus allowing the identification of metabolic processes affected by NO. At early time points after treatment, NO scavenged superoxide anion and induced the nitration and the S-nitrosylation of proteins. These events preceded an extensive though transient metabolic reprogramming at 6 h after NO treatment, which included enhanced levels of polyamines, lipid catabolism and accumulation of phospholipids, chlorophyll breakdown, protein and nucleic acid turnover and increased content of sugars. Accordingly, lipid-related structures such as root cell membranes and leaf cuticle altered their permeability upon NO treatment. Besides, NO-treated plants displayed degradation of starch granules, which is consistent with the increased sugar content observed in the metabolomic survey. The metabolic profile was restored to baseline levels at 24 h post-treatment, thus pointing up the plasticity of plant metabolism in response to nitroxidative stress conditions.
Highlights
Most of the studies quantifying NO production in plants measure NO emission, which is just a fraction of the total NO synthesized inside cells
The recent implementation of techniques using microchip electrophoresis and laser-induced fluorescence detection allowed reporting intracellular concentrations of NO around 0.6 mM for human Jurkat cells that can be increased to 1.5 mM under stress conditions induced by lipopolysaccharides[37]
No such approach has been implemented for plant cells
Summary
A statistically significant increase in the amount of lipid, carbohydrate, amino acid and nucleotide categories of analyzed metabolites was detected in plants by 6 h after exposure to NO (Fig. 1a). The metabolites showed significant alteration in their endogenous levels by 6 h after exposure to NO (Fig. 1a and Supplementary Table S1).
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