Iron (Fe) is abundant in soils but with a poor availability for plants, especially in calcareous soils. To favor its acquisition, plants develop morphological and physiological responses, mainly in their roots, known as Fe deficiency responses. In dicot plants, the regulation of these responses is not totally known, but some hormones and signaling molecules, such as auxin, ethylene, glutathione (GSH), nitric oxide (NO) and S-nitrosoglutathione (GSNO), have been involved in their activation. Most of these substances, including auxin, ethylene, GSH and NO, increase their production in Fe-deficient roots while GSNO, derived from GSH and NO, decreases its content. This paradoxical result could be explained with the increased expression and activity in Fe-deficient roots of the GSNO reductase (GSNOR) enzyme, which decomposes GSNO to oxidized glutathione (GSSG) and NH3. The fact that NO content increases while GSNO decreases in Fe-deficient roots suggests that NO and GSNO do not play the same role in the regulation of Fe deficiency responses. This review is an update of the results supporting a role for NO, GSNO and GSNOR in the regulation of Fe deficiency responses. The possible roles of NO and GSNO are discussed by taking into account their mode of action through post-translational modifications, such as S-nitrosylation, and through their interactions with the hormones auxin and ethylene, directly related to the activation of morphological and physiological responses to Fe deficiency in dicot plants.
Keywords: Fe deficiency responses; GSNO reductase; S-nitrosoglutathione; dicotyledonous; ethylene; glutathione; iron; nitric oxide.