AhGSNOR negatively regulates Al-induced programmed cell death by regulating intracellular NO and redox homeostasis

Abstract

Abstract Aims The toxicity of aluminum (Al) in acidic soil inhibits plant development and reduces crop yields. Programmed cell death (PCD) is one of the important mechanisms in the plant response to Al toxicity. However, it is yet unknown if S-nitrosoglutathione reductase (GSNOR) provides Al-toxicity tolerance. Methods AhGSNOR was cloned and its expression was analyzed. The NO content, SNO content, and GSNOR activity in roots of wild type and AhGSNOR transgenic tobacco under different Al stress conditions were detected, as well as root elongation, cell death, antioxidant enzyme activity, H2O2 level and lipid peroxidation degree. The relationship between AhGSNOR and TRXh was also explored. Results Transcription and protein expression of AhGSNOR were both induced by Al stress. Both AhGSNOR-overexpressing transgenic and antisense tobacco plants exhibited a late flowering phenotype compared to the wild type, implying that stability of AhGSNOR expression is required for normal growth and development. Moreover, AhGSNOR overexpression reduced Al-induced nitric oxide (NO) and S-nitrosothiol accumulation, the inhibitory effect of Al stress on root elongation and the degree of cell death, and enhanced antioxidant enzyme activity to effectively remove hydrogen peroxide. In addition, AhTRXh directly interacted with AhGSNOR in peanut in vitro and in vivo. Expression of NtTrxh3 in AhGSNOR-overexpressing transgenic plants was significantly upregulated. Conclusions These results suggested that AhGSNOR was a negative regulatory factor of Al-induced PCD and improved plant Al-tolerance by modulating intracellular NO and redox homeostasis.