Both plant hormones and some
Both plant hormones and some second messengers are involved in Fe-deficiency-related responses in plants (Kobayashi and Nishizawa, 2012). Among these second messengers, nitric oxide (NO) accumulation was induced by Fe deficiencies in tomato and Arabidopsis roots, and it acts as the downstream signal of auxin, upregulating the Fe-acquisition genes (Chen et al., 2010; Graziano and Lamattina, 2007). FIT links NO and Fe signaling through the post-translational regulation of NO accumulation, suggested that the stability and activity of FRO may also be regulated by the signal molecule NO (Meiser et al., 2011). Additionally, exogenous applications of NO may have protective effects on Fe-deficiency-induced chlorosis (Kong et al., 2014) and oxidative stress (Sun et al., 2007), and impact the Colistin Methanesulfonate sodium salt levels of Fe-uptake- and transport-related genes (Zhu et al., 2016) in plants. Although NO plays a crucial role in Fe-deficiency responses, long-term exposure, or exposure to high NO concentrations, it usually leads to the permanent inhibition of some normal physiological mechanisms and stress responses (Leterrier et al., 2011). NO has been described as an endogenous RNS signal that mediates responses to many physiological and developmental processes, as well as to various stresses, in all higher organisms (Gadelha et al., 2017; Hasanuzzaman et al., 2018). NO signaling is involved in the regulation of both gene transcription and post-translational modifications of proteins (Astier et al., 2018). NO exerts these functions directly or through a group of derived molecules, designated as RNS, that are involved in post-translational modifications, including S-nitrosylation of thiol groups, nitration of tyrosine, and binding to metal centers, during cell signaling events (Fancy et al., 2016; Leterrier et al., 2011). A growing number of plant proteins have been described as targets of post-translational modifications by NO-mediated S-nitrosylation under stress conditions (Fancy et al., 2016; Zhang et al., 2017b). Putative analyses in Arabidopsis, rice, and wheat separately revealed 30, 15, and 6 candidate proteins that are regulated by S-nitrosylation under Fe-deficiency stress (Darbani et al., 2013). Recently, the formation of S-nitrosoglutathione (GSNO) by a spontaneous reaction of NO with reduced glutathione has aroused great interest. GSNO may be a NO donor or reservoir that is involved in transferring NO moieties to thiol groups or in the transnitrosylation processes (Leterrier et al., 2011). Thus, the GSNO levels may reflect the level of intracellular protein S-nitrosylation, which is mainly regulated by the activity of the S-nitrosoglutathione reductase (GSNOR) (Leterrier et al., 2011). The results of the GSNOR-catalyzed reaction are the depletion of GSNO levels and a reduced likelihood of S-nitrosothiol (SNO) formation through transnitrosylation. Therefore, GSNOR has emerged as the critical enzyme responsible for the modulation of NO-mediated signaling pathways (Frungillo et al., 2013). Oxidative stress responses have been described as major physiological switches during stress conditions. However, knowledge regarding the RNS-derived effects on abiotic stress physiology is still limited. Plants exhibit remarkable nitrosative changes in response to stressful environmental conditions (Ziogas et al., 2013). The GSNOR mutant hot5 in Arabidopsis shows a weaker thermotolerance and greater NO concentration compared with wild type (WT), whereas GSNOR overexpression inhibited NO generation, suggesting that GSNOR’s activity in the stress response involves regulating NO homeostasis (Lee et al., 2008). Several abiotic stresses, including heat, cold, mechanical, continuous dark, and de-etiolation, can generally induce GSNOR’s activity in studied plants, which pointed to critical roles for GSNOR during normal plant development and in plant responses to stress conditions (Kubienová et al., 2014).