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    • Glycogen synthase kinase GSK a serine threonine kinase has b

    2021-09-17

    Glycogen synthase kinase-3 (GSK-3), a serine/threonine kinase, has been confirmed to be involved in some biological processes in NaCl or wound-treated plants (Chen et al., 2003, Hai et al., 2001, Jonak et al., 2000). NO has been recently recognized as a vital signaling compound in plants. The NO donor, sodium nitroprusside (SNP) induced activation of GSK-3 in the kidneys of diabetic mice (Mariappan et al., 2014). Additionally, treatment with another NO donor, s-nitroso-L-glutathione (GSNO), led to a significant decrease in phosphorylation of GSK-3 at serine 9 and an increase in phosphorylation of glycogen synthase, an endogenous substrate of GSK-3 in pancreatic β-cells (Tanioka et al., 2011). These data indicate that NO, as a critical signaling molecule, modulates GSK-3 activation. Both GSK-3 activation and isoflavone accumulation result from defense reactions. Nevertheless, whether GSK-3 is involved in mediation of isoflavone production by endogenous NO in plants under UV-B radiation remains to be determined. Usually, the downstream signaling transduction of NO requires involvement of cGMP (Misra, Misra, & Singh, 2010). Accordingly, when human neuroblastoma (SH-SY5Y) TDZD-8 were treated with cGMP, phosphorylation of GSK-3 was significantly elevated (Sanyal, Lochmatter, Preußner, & Pfeifer, 2013), indicating the essential role of cGMP in regulating GSK-3 phosphorylation. Moreover, the intracellular biological function of cGMP is usually dependent on protein kinase G (PKG; Lincoln, Dey, & Sellak, 2001), which has been identified as one of the major intracellular receptors for cGMP (Komalavilas, Shah, Jo, & Lincoln, 1999). KT5823 (a PKG inhibitor) significantly weakened sildenafil-enhanced phosphorylation of GSK-3 in adult male mice (Das, Xi, & Kukreja, 2008). This provides evidence for the involvement of the PKG pathway in GSK-3 phosphorylation. Relatively little is known about the role of the cGMP/PKG pathway in NO-induced GSK-3 activation under UV-B radiation in plants. Recently, we reported that cGMP, as a second messenger in NO signaling, is involved in UV-B stress-stimulated isoflavone production in soybean sprouts (Jiao et al., 2016). The effects of GSK-3 on NO-cGMP-activated isoflavone synthesis in soybean sprouts under UV-B radiation requires further investigation. Soybean sprouts, as traditional vegetables, have been consumed for centuries in Asian countries. Germination is known to increase levels of essential nutrients of soybean seeds like isoflavones (Shi, Nam, & Ma, 2010). The objectives of this study were to investigate the role of the NO-cGMP-GSK-3 pathway in UV-B exposure-activated isoflavone production in soybean sprouts and to explore the relevant enzymatic and molecular mechanisms. This work provides a better understanding of the molecular mechanisms underlying the synthesis of health-promoting substances and the functional properties of soybean sprouts, leading to practical implications for future commercial production of functional foods in the agricultural and food industries.
    Materials and methods
    Results
    Discussion UV-B stress significantly enhanced gene (Fig. 1) and protein (Fig. 3) expression of GSK-3 in soybean sprouts, indicating that GSK-3 was activated by UV-B treatment. However, cPTIO (a NO-scavenger) inhibited the UV-B radiation-activated expression. Addition of SNP (a NO donor) abrogated this inhibition. SNP used alone also induced an elevation in gene (Fig. 1) and protein (Fig. 3) expression of GSK-3. The data demonstrated that NO, as an essential signal, was involved in UV-B radiation-triggered GSK-3 activation in soybean sprouts. Accordingly, in murine kidney cells, NO activates GSK-3 by reducing Ser-9 phosphorylation (Mariappan et al., 2014). Additionally, GSK-3 Ser-9 phosphorylation is modulated by Akt and the extracellular signal-regulated kinase, ERK (Mariappan et al., 2008, Welsh and Proud, 1993), which is in turn, regulated by Tyr-416 phosphorylation of Src and Tyr-402 phosphorylation of proline-rich tyrosine kinase 2 (Pyk2; Goc et al., 2014, Sonomura et al., 2012). Thus, NO may inhibit Akt and ERK via down regulation of Src and Pyk2, leading to GSK-3 activation. In addition, in obese, diabetic mice, iNOS activates GSK-3 by s-nitrosylation of cysteine 330 (Shimizu, Kinoshita, & Kaneki, 2007), from which we can speculate that UV-B radiation-induced NO biosynthesis possibly activates GSK-3 through elevation of s-nitrosylation at cysteine 330.