S-nitrosation

S-nitrosation arises through multiple, context-dependent biochemical pathways governed by the redox environment and the availability of reactive nitrogen species (RNS) (Lin et al., 2025). Direct nitrosation is primarily mediated by NO-derived oxidized intermediates, such as dinitrogen trioxide (N2O3), which efficiently target cysteine residues under aerobic conditions (Wei et al., 2024; Lin et al., 2025). In vivo, transnitrosation constitutes a dominant mechanism, whereby NO groups are transferred from low-molecular-weight S-nitrosothiols, particularly GSNO, or from S-nitrosated proteins to specific cysteine residues, enabling amplification and propagation of NO signaling (Wei et al., 2024; Liu et al., 2024). Transition metals, including iron and copper, can further facilitate localized nitrosation reactions (Lin et al., 2025). Site selectivity is dictated by cysteine physicochemical properties -such as thiol pKa, solvent accessibility, and the surrounding amino acid environment- ensuring that S-nitrosation targets defined protein subsets rather than occurring indiscriminately (Pande et al., 2022; Lin et al., 2025). S-nitrosation is dynamically reversible. Thioredoxins (Trx) directly catalyze denitrosation of specific protein targets, whereas GSNOR regulates SNO homeostasis indirectly through GSNO degradation (Jedelská et al., 2020; Treffon et al., 2021; Liao et al., 2023; Lin et al., 2025). In addition, NADPH-dependent GSNO catabolism mediated by aldo-keto reductases (AKRs) introduces an additional regulatory layer (Jedelská et al., 2020; Treffon et al., 2021; Das et al., 2025). Together, these systems establish tight spatiotemporal control over NO signaling.

Fig. 1. Mechanisms and regulation of protein S-nitrosation in plants. NO and NO-derived reactive species promote S-nitrosation either directly or via transnitrosation through low-molecular-weight S-nitrosothiols, primarily GSNO. Target specificity is determined by the local protein environment and cysteine reactivity. The S-nitrosation status is dynamically regulated by denitrosation systems, including Trx/thioredoxin reductase and GSNOR, as well as alternative GSNO catabolic pathways such as aldo-keto reductases (AKRs). This balance ensures reversible and selective NO-dependent signaling. Adapted from: Lin et al., 2025; Liao et al., 2023; Wei et al., 2024; Liu et al., 2024; Das et al., 2025.

S-nitrosation is integral to the regulation of plant growth, development, and signaling networks through its effects on enzymes, transcription factors, and signaling proteins (Liu et al., 2024; Lin et al., 2025). It governs processes such as germination, root development, flowering, and senescence, and modulates gene expression by altering transcription factor activity and DNA-binding capacity (Liao et al., 2023; Wei et al., 2024). At the systems level, S-nitrosation operates at the interface of hormone signaling, redox regulation, and stress adaptation. It contributes to auxin and abscisic acid (ABA) pathways and modulates defense responses through NO/ROS crosstalk (Kolbert et al., 2019; Pande et al., 2022; Sedlářová et al., 2025). Moreover, it interacts with other post-translational modifications, including phosphorylation, tyrosine nitration, and glutathionylation, forming interconnected regulatory networks. The balance between S-nitrosation and denitrosation defines cellular redox homeostasis. GSNO functions as a central NO reservoir, while GSNOR and thioredoxin systems regulate its turnover and protein SNO levels (Jedelská et al., 2020; Treffon et al., 2021; Das et al., 2025). Disruption of this balance leads to nitrosative stress and impaired cellular function, whereas coordinated interactions with reactive oxygen species (ROS) enable fine-tuned signaling responses (Wei et al., 2024; Liu et al., 2024).

Fig. 2. Functional roles of protein S-nitrosation in plant physiology. S-nitrosation acts as a central regulatory mechanism influencing multiple biological processes, including growth and development, hormone signaling (auxin, abscisic acid, salicylic acid), chloroplast function and metabolism, immune responses, and adaptation to abiotic stress. By modulating protein activity, localization, and turnover, S-nitrosation integrates nitric oxide signaling with redox homeostasis and plant stress responses. Adapted from: Liao et al., 2023; Liu et al., 2024; Wei et al., 2024; Lin et al., 2025; Sedlářová et al., 2025.