Hydrogen sulfide and nitric oxide regulate the adaptation to iron deficiency through affecting Fe homeostasis and thiol redox modification in Glycine max seedlings

Iron (Fe) is a vital microelement required for the growth and development of plants. Hydrogen sulfide (H2S) and nitric oxide (NO), as messenger molecules, participated in the regulation of plant physiological processes. Here, we studied the interaction effects of H2S and NO on the adaptation to Fe deficiency in Glycine max L. Physiological, biochemical and molecular approaches were conducted to analyze the role of H2S and NO in regulating the adaptation to Fe deficiency in soybean. We found that H2S and NO had obvious rescuing function on the Fe deficiency-induced the plant growth inhibition, which was significantly correlated with the increase in Fe content in the leaves, stems, and roots of soybean. Meanwhile, H+-flux, ferric chelate reductase (FCR) activity, and root apoplast Fe content were significantly affected by H2S and NO. Under Fe deficiency conditions NO and H2S regulated the expression of genes related to Fe homeostasis. Moreover, photosynthesis (Pn) and photosystem II (PSII) efficiency were enhanced by H2S and NO, and thiol redox modification was important for regulating the adaptation of Fe deficiency. The aforementioned affirmative influences caused by H2S and NO were also totally reversed by cPTIO (a NO scavenger). Our results suggested that H2S might act upstream of NO in response to Fe deficiency by affecting the Fe homeostasis enzyme activities and gene expression, and by promoting Fe accumulation in plant tissues as well as by enhancing thiol redox modification and photosynthesis in soybean plants. •H2S and NO had significant rescuing effects on the Fe deficiency-induced inhibition of plant growth.•H+-flux, ferric chelate reductase (FCR) activity, and root apoplast Fe contents were significantly affected by H2S and NO.•H2S and NO regulated the gene expression of Fe homeostasis in soybean plants under Fe deficiency conditions.•H2S and NO regulated the adaptation of Fe deficiency by affecting thiol redox modification and photosynthesis.