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  • SNS-032 br Consequence physiological function of ROS depende

    2022-07-01


    Consequence/physiological function of ROS-dependent inhibition of GSNOR Plants response to environmental changes induced by abiotic and biotic factors by enhanced accumulation of ROS resulting in temporary imbalance of the cellular redox homeostasis. This as oxidative stress/burst termed event triggers both signaling events and damaging processes [47]. Such a change in ROS SNS-032 and the associated shift in the redox state are mainly sensed by distinct redox-sensitive protein amino acids. Post-translational protein modifications arising from interaction with ROS are oxidation of sulphur-containing residues (cysteine, methionine) and aromatic residues (tyrosine, tryptophan), carbonylation reactions and formation of disulfide bridges [48], [49]. Such modification can affect the function/activity of proteins and therefore represent an important part of ROS signaling function. A similar function is known for reactive nitrogen species and NO/SNO-signaling is also involved in biotic and abiotic stress responses. GSNOR activity controls intracellular levels of GSNO and S-nitrosylated proteins and the physiological importance of GSNOR in fine-tuning ·No/SNO levels during many stress responses and in plant growth and development is well described. Interestingly, GSNOR activity is inhibited by H2O2in-vitro or paraquat in-vivo Kovacs et al. [36], providing evidence for crosstalk between ROS and NO signaling. The physiological function of ROS-dependent inhibition of GSNOR might be related to a protective role against oxidative stress. Inhibition of GSNOR or a knock-out of GSNOR resulted in enhanced levels of NO/SNO. Moreover, SNO levels increased more than twofold in WT plants after paraquat treatment providing evidence for ROS-induced inactivation of GSNOR in-vivo. Furthermore, Co-treatment of ·No donor sodium nitroprusside and paraquat during germination of WT plants resulted in increased resistance to paraquat supporting the hypothesis that enhanced levels of ·No/SNOs due to inhibition of GSNOR protects against oxidative stress [50]. A protective effect of ·No against paraquat-induced oxidative stress was also described in potato and rice after incubation with ·No-releasing compounds [51], [52]. ·No can fulfill its protective function in different ways. On one side, paraquat-treated gsnor mutant accumulates lower amount of H2O2 than the WT plant supporting a direct scavenging function of ·No to decrease excess level of ROS species. Peroxynitrite (ONOO−) formation can be a mechanism to consume superoxide thereby protecting biomolecules from oxidation and preventing further ROS production [53], [54], [55], [56]. Reciprocal scavenging of ·No and O2−. leads to the formation of ONOO−, which does not appear to be particularly toxic in plants [57], [58]. In soybean cells it was demonstrated that ONOO- is not a determining factor of hypersensitive cell death, but the common action of ·No and H2O2. Since tyrosine nitration level - a marker for ONOO- production - in the paraquat-treated gsnor plants is reduced, it is also thinkable that the turnover of ONOO- is affected by excess ·No/SNO. Moreover, ONOO- itself could lower H2O2 production by inhibiting several isoforms of SOD [59]. ROS-dependent inhibition of GSNOR results in accumulation of GSNO, which could be decomposed in presence of O2- to radical glutathione and ONOO-. As consequence, ONOO- would accumulate and inhibit SOD-dependent production of H2O2[60]. Another example for a direct effect of ·No/SNO on ROS producing systems is the inhibition of NADPH oxidase activity by S-nitrosylation, resulting in the reduction in ROS biosynthesis during immune responses [61]. The activation of the antioxidative system represents another protective action of ·No/SNO against ROS burst. Glutathione is the major low molecular weight thiol, which is crucial to maintain cellular redox balance and which is produced rapidly in response to many stress situations. Exogenously supplied gaseous ·No or enhanced endogenous ·No/SNO levels stimulate the GSH biosynthesis pathway in Arabidopsis Kovacs et al. [36]. Moreover, a higher amount of GSH was measured in roots of Medicago truncatula[62] and maize leaves [63] in response to GSNO and SNP treatment, respectively. At least for the two latter cases, increased expression of the γ-glutamylcysteine synthetase and GSH synthetase gene was measured concluding that ·No regulates GSH production on transcriptional level. Besides enhanced GSH production, increased activity of glutathione reductase has been observed in plants with enhanced ·No/SNO levels, ensuring the provision with enough reducing equivalents for response to oxidative stress [36]. Recent paper has provided evidence that S-nitrosylation of Arabidopsis ascorbate peroxidase 1 (APX1) enhances its activity to scavenge H2O2 and to increase resistance to oxidative stress [64]. S-Nitrosylation of pea APX also enhanced its enzyme activity in saline stress [65].