Overexpression of S-nitrosoglutathione reductase alleviated iron-deficiency stress by regulating iron distribution and redox homeostasis.

Iron (Fe) is an essential micronutrient element for plant growth. The S-nitrosoglutathione reductase (GSNOR) gene's functions under Fe-deficiency conditions are not well understood. Here, GSNOR expression was induced by Fe deficiency in tomato (Solanum lycopersicum L.) leaves and roots, while its overexpression alleviated chlorosis under Fe-deficiency conditions. GSNOR overexpression positively regulated the Fe distribution from root to shoot, which might result from the transcriptional regulation of genes involved in Fe metabolism. Additionally, the overexpression of GSNOR maintained redox homeostasis and protected chloroplasts from Fe-deficiency-related damage, resulting in a greater photosynthetic capacity. As a nitric oxide regulator, GSNOR's overexpression decreased the excessive accumulation of nitric oxide and S-nitrosothiols during the Fe deficiency, and maintained the homeostases of reactive oxygen species and reactive nitrogen species. Moreover, GSNOR overexpression, probably at the level of genes and proteins, along with protein S-nitrosylation, promoted Fe uptake and regulated the shoot/root Fe ratio under Fe-deficiency conditions.