Role of glycine in improving the ionic and ROS homeostasis during NaCl stress in wheat.

Nine-day-old wheat seedlings were treated with NaCl at 75, 150, and 225 mM for 15 days in the absence or presence of 5 mM glycine. NaCl particularly at 150 and 225 mM led to significant reductions in fresh and dry weights, chlorophylls, carotenoids, Ca(2+), K(+), and K(+)/Na(+) ratio. Contrarily, there were significant accumulations in Na(+), malondialdehyde (MDA), H2O2, soluble sugars, and proline concomitant with inhibitions in enzymatic and non-enzymatic antioxidants and in Rubisco. In the meantime, the transcript level of alternative oxidase (AOX) was highly upregulated by NaCl; the upregulation was greatest with the lowest concentration. However, the transcript level of H(+)/Na(+) antiporter exchanger (NHX1) was decreased by 75 and 150 mM NaCl but increased by 225 mM. Similarly, the transcript level of salt overly sensitive 1 (SOS1) was upregulated by only 225 mM. Nonetheless, the application of glycine mostly overcame the varied impacts of NaCl on growth, MDA, H2O2, pigments, metabolites, and elements. Moreover, glycine elevated enzymatic and non-enzymatic antioxidants to reach most likely the levels of the respective control. On the contrary, much induction was detected in Rubisco. The transcript levels of AOX, NHX1, and SOS1 were further upregulated; the upregulation of AOX was most pronounced with the highest NaCl concentration in the presence of glycine and only with 75 and 150 mM NaCl for NHX1 and SOS1. The increase in antioxidants concomitant with the decrease in MDA and H2O2 reveals that ROS scavenging system became more efficient in NaCl-treated wheat following glycine application, concluding that glycine could ameliorate wheat tolerance to salinity. Moreover, lowering Na(+) by glycine and mitigation of the decreased K(+)/Na(+) ratio synchronous with recovery in growth reduction and stimulation of AOX, NHX1 and SOS1 may emphasize the role of glycine in stimulating gene expression for raising wheat tolerance to NaCl.