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  • The Fe deficiency treatment significantly increased the

    2021-10-16

    The Fe-deficiency treatment significantly increased the shoot/root Fe ratios in both WT and transgenic lines (Fig. 5C), which implied that the Fe distribution from root to shoot may be an adaptive mechanism or stress response in tomato plants. Thus, the overexpression of GSNOR had a positive effect on tomato plants, decreasing the detrimental effects of the Fe deficiency by regulating the Fe distribution. SlOPT9 is a homolog of AtOPT3, which is a plasma membrane transporter capable of regulating both shoot-to-root Fe signaling and Fe redistribution (Zhai et al., 2014). When the lack of Fe is signaled, the greater vivo vu of OPT9 in WT might help the plant acquire more Fe (Fig. 6A). Additionally, OPT9, as well as the transport system mediating Fe’s partitioning, which reduces the urgent need for Fe, led to a mild upregulation of OPT9 expression in the OE-2 line (Fig. 6A). OPT9 may be regulated by S-nitrosylation as predicted by GSP-SNO software. In addition, other transporter family members could also be S-nitrosylated, which could lead to abundant levels of nitrosylation being involved in regulating Fe transportation. In accordance with the nitrosylation-based affinity, the same protein may have different nitrosylation levels under different conditions. Thus, FRO8, NRAMP2, and NRAMP3 (Fig. 6A) had similar change trends as that of OPT9, at the transcriptional level, but they changed to different degrees. FROs reduce Fe3+ chelation to form soluble ferrous Fe, and FRO8 plays an essential role in Fe delivery to mitochondria. Thus, it might contribute to mitochondrial Fe homeostasis, which was detected in a mitochondrial proteomics study (Heazlewood et al., 2004). Additionally, VIT encodes a vacuolar iron transporter that imports Fe into the vacuole (Sun et al., 2006); it is also upregulated during Fe deficiency, indicating that NRAMP is not only involved in the acquisition and recycling vacuolar Fe but also acts in limiting Fe storage in vacuoles. Moreover, the fold structure of the VIT gene does not vary as much as those of the NRAMP2 and NRAMP3 genes, which indicates that more Fe was transferred out of the vacuoles under Fe-deficiency conditions. In addition, NRAMP2 and NRAMP3 could be S-nitrosylated (Supplemental Table 2), which means that RNS may participate in the response to Fe deficiency at the level of post-transcriptional modification. In addition to Fe compartmentalization and translocation, the effect of GSNOR influences Fe uptake in roots. In response to the Fe deficiency, a reduction-based mechanism was employed by inducing ferric-chelate reductase at the root plasma membrane to enhance Fe uptake, and the low-Fe-inducible FCR is the limiting enzyme in the acquisition of Fe. Meanwhile, SlFRO1, a homolog of AtFRO2, encoding ferric-chelate reductase and functioning in the reduction of ferric to ferrous Fe on the root surface (Connolly et al., 2003, Robinson 1999), participates in an essential process for Fe uptake in Strategy I plants (Brumbarova and Bauer, 2005). As shown in Fig. 7, in addition to gene regulation, the post-transcriptional modification may play a pivotal important role in regulating protein functions, leading to the varied activity of FCR in the OE-2 line under Fe-deficiency conditions. In addition, multiple proteins were predicted as having S-nitrosylation sites, and the same protein can have varying degrees of S-nitrosylation, forming the post-transcriptional regulatory complex. Based on our results and analyses, a schematic illustration of a possible mechanism for SlGSNOR regulation of tomato tolerance to Fe deficiency was produced (Fig. 8). The function of GSNOR is dependent on the role of FRO1 in Fe reduction, and it promotes Fe uptake and transportation, as well as redox homeostasis. The lower level of ROS generation under Fe-deficiency conditions in GSNOR-overexpressing tomato leaves was closely correlated with the GSNOR-modulated RNS level. Based on the combined regulatory effects of Fe metabolism and free radicals, the structure of the chloroplast was maintained, as was normal photosynthesis.