S-Nitrosylation and Nitric Oxide Signaling in Plant Stress Responses
Summary
Plants endure a wide array of environmental stresses, from drought and salinity to nutrient imbalance and pathogen attack. Central to many adaptive responses is nitric oxide (NO), a small, diffusible radical that orchestrates signal transduction through reversible post-translational modification of proteins, most notably S-nitrosylation. This modification involves covalent attachment of NO to reactive cysteine residues, thereby modulating enzyme activity, subcellular localisation and protein–protein interactions. Through dynamic interplay with reactive oxygen species (ROS), plant hormones and redox buffers, NO fine-tunes stress perception and downstream defence pathways. S-nitrosylation regulates processes as diverse as hormonal cross-talk, antioxidant enzyme function, ion transport and transcription factor stability, thereby influencing stomatal aperture, osmolyte accumulation, cell death programmes and systemic acquired resistance. Advances in proteomic technologies have greatly expanded the catalogue of S-nitrosylated targets, revealing intricate networks that underpin redox homeostasis. Understanding how NO synthesis pathways—principally nitrate reductase and other enzymatic sources—are integrated with scavenging systems continues to illuminate the balance between signalling and nitro-oxidative damage. Practically, manipulation of NO metabolism and S-nitrosylation holds promise for engineering stress-tolerant crops with enhanced yield stability under challenging environments.
Research from Nature Portfolio
Recent studies have harnessed innovative proteomic techniques to quantify the in vivo dynamics of S-nitrosylation at unprecedented scale. A highly sensitive fluorous affinity tag-switch approach profiled over 2,000 S-nitrosylated peptides in wild-type and mutant Arabidopsis, identifying regulatory sites on key endoplasmic reticulum oxidoreductases that control protein folding and stress resilience. Biochemical and genetic validation revealed that S-nitrosylation of a specific cysteine causes conformational changes that enhance enzyme activity, thus linking NO signalling to endoplasmic reticulum function. In parallel, work on seed germination uncovered how NO modulates hormone interplay by targeting a bZIP transcription factor. S-nitrosylation at a single conserved cysteine accelerates its degradation via specific E3 ligases, overcoming abscisic acid-mediated growth arrest and promoting seedling establishment. These findings illustrate the precision of NO-driven post-translational control over developmental and stress-responsive transcriptional hubs.
S-Nitrosylation and Nitric Oxide Signaling in Plant Stress Responses publication trend
The graph below shows the total number of articles in s-nitrosylation and nitric oxide signaling in plant stress responses across all publications each year (not limited to Nature Index journals).
Technical terms
S-nitrosylation: reversible covalent addition of an NO moiety to a cysteine thiol on a protein, altering its function or interactions.
Nitric oxide (NO): a gaseous free radical that serves as a diffusible signalling molecule in plants, modulating stress and developmental pathways.
S-nitrosothiol (SNO): a stable reservoir of NO formed by S-nitrosylation, capable of transnitrosation and long-distance signalling.
Reactive oxygen species (ROS): partially reduced oxygen derivatives that act as signalling intermediates or cause oxidative damage when unregulated.
References
- FAT-switch-based quantitative S-nitrosoproteomics reveals a key role of GSNOR1 in regulating ER functions. Nature Communications (2023).
- S-nitrosylation triggers ABI5 degradation to promote seed germination and seedling growth. Nature Communications (2015).
- SlTrxh functions downstream of SlMYB86 and positively regulates nitrate stress tolerance via S-nitrosation in tomato seedling. Horticulture Research (2024).
- Assessment of Subcellular ROS and NO Metabolism in Higher Plants: Multifunctional Signaling Molecules. Antioxidants (2019).
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