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Iron is one of the most important micronutrients in plants as it is involved in many cellular functions (e.g., photosynthesis and respiration). Any defect in iron availability will affect plant growth and development as well as crop yield and plant product quality. Thus, iron homeostasis must be tightly controlled in order to ensure optimal absorption of this mineral element. Understanding mechanisms governing iron homeostasis in plants has been the focus of several studies during the past 10 years. These studies have greatly improved our understanding of the mechanisms involved, revealing a sophisticated iron-dependent transcriptional regulatory network. Strikingly, these studies have also highlighted that this regulatory web relies on the activity of numerous transcriptional regulators that belong to the same group of transcription factors (TF), the bHLH (basic helix-loop-helix) family. This is best exemplified in Arabidopsis where, to date, 16 bHLH TF have been characterized as involved in this process and acting in a complex regulatory cascade. Interestingly, among these bHLH TF some form specific clades, indicating that peculiar function dedicated to the maintenance of iron homeostasis, have emerged during the course of the evolution of the green lineage. Within this mini review, we present new insights on the control of iron homeostasis and the involvement of bHLH TF in this metabolic process.

Summary Iron (Fe) homeostasis is crucial for all living organisms. In mammals, an integrated posttranscriptional mechanism couples the regulation of both Fe deficiency and Fe excess responses. Whether in plants an integrated control mechanism involving common players regulates responses both to deficiency and to excess is still to be determined. In this study, molecular, genetic and biochemical approaches were used to investigate transcriptional responses to both Fe deficiency and excess. A transcriptional activator of responses to Fe shortage in Arabidopsis, called bHLH105/ILR3, was found to also negatively regulate the expression of ferritin genes, which are markers of the plant's response to Fe excess. Further investigations revealed that ILR3 repressed the expression of several structural genes that function in the control of Fe homeostasis. ILR3 interacts directly with the promoter of its target genes, and repressive activity was conferred by its dimerisation with bHLH47/PYE. Last, this study highlighted that important facets of plant growth in response to Fe deficiency or excess rely on ILR3 activity. Altogether, the data presented herein support that ILR3 is at the centre of the transcriptional regulatory network that controls Fe homeostasis in Arabidopsis, in which it acts as both transcriptional activator and repressor.

Glutathione transferases (GSTs) belong to a ubiquitous multigenic family of enzymes involved in diverse biological processes including xenobiotic detoxification and secondary metabolism. A canonical GST is formed by two domains, the N-terminal one adopting a thioredoxin (TRX) fold and the C-terminal one an all-helical structure. The most recent genomic and phylogenetic analysis based on this domain organization allowed the classification of the GST family into 14 classes in terrestrial plants. These GSTs are further distinguished based on the presence of the ancestral cysteine (Cys-GSTs) present in TRX family proteins or on its substitution by a serine (Ser-GSTs). Cys-GSTs catalyze the reduction of dehydroascorbate and deglutathionylation reactions whereas Ser-GSTs catalyze glutathione conjugation reactions and eventually have peroxidase activity, both activities being important for stress tolerance or herbicide detoxification. Through non-catalytic, so-called ligandin properties, numerous plant GSTs also participate in the binding and transport of small heterocyclic ligands such as flavonoids including anthocyanins, and polyphenols. So far, this function has likely been underestimated compared to the other documented roles of GSTs. In this review, we compiled data concerning the known enzymatic and structural properties as well as the biochemical and physiological functions associated to plant GSTs having a conserved serine in their active site.

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Iron (Fe) is a major micronutrient and is required for plant growth and development. Nongrass species have evolved a reduction-based strategy to solubilize and take up Fe. The secretion of Fe-mobilizing coumarins (e.g. fraxetin, esculetin and sideretin) by plant roots plays an important role in this process. Although the biochemical mechanisms leading to their biosynthesis have been well described, very little is known about their cellular and subcellular localization or their mobility within plant tissues. Spectral imaging was used to monitor, in Arabidopsis thaliana, the in planta localization of Fe-mobilizing coumarins and scopolin. Molecular, genetic and biochemical approaches were also used to investigate the dynamics of coumarin accumulation in roots. These approaches showed that root hairs play a major role in scopoletin secretion, whereas fraxetin and esculetin secretion occurs through all epidermis cells. The findings of this study also showed that the transport of coumarins from the cortex to the rhizosphere relies on the PDR9 transporter under Fe-deficient conditions. Additional experiments support the idea that coumarins move throughout the plant body via the xylem sap and that several plant species can take up coumarins present in the surrounding media. Altogether, the data presented here demonstrate that coumarin storage and accumulation in roots is a highly complex and dynamic process.

Iron (Fe) is an important micronutrient for plant growth and development but any excess of Fe is toxic because of the Fe-dependent generation of reactive oxygen species (ROS). Thus, Fe homeostasis must be tightly regulated. In Arabidopsis thaliana, a cascade of transcription factors has been identified as involved in the regulation of this process by modulating the expression of genes related to Fe uptake, transport, and storage. Recently, it was demonstrated that in response to Fe deficiency, bHLH121/URI (UPSTREAM REGULATOR OF IRT1) directly activates the expression of several genes involved in this regulatory network. It was also shown that bHLH121 interacts with ILR3 (bHLH105) and its homologs. Herein it is shown that bHLH121 is necessary for the expression of the main markers of the plant responses to Fe excess, the ferritin genes (i.e. FER1, FER3, and FER4). bHLH121 regulates ferritin genes expression by directly binding to their promoters, at the same locus than the ILR3-PYE repressive complex. Therefore, this study highlight that bHLH121, PYE, and ILR3 form a chain of antagonistic switches that regulate the expression of ferritin genes. The implication of this finding is discussed.

Among the mineral nutrients that are required for plant metabolism, iron (Fe) and sulphur (S) play a central role as both elements are needed for the activity of several proteins involved in essential cellular processes. A combination of physiological, biochemical and molecular approaches was employed to investigate how S availability influences plant response to Fe deficiency, using the model plant Arabidopsis thaliana. We first observed that chlorosis symptom induced by Fe deficiency was less pronounced when S availability was scarce. We thus found that S deficiency inhibited the Fe deficiency induced expression of several genes associated with the maintenance of Fe homeostasis. This includes structural genes involved in Fe uptake (i.e. IRT1, FRO2, PDR9, NRAMP1) and transport (i.e. FRD3, NAS4) as well as a subset of their upstream regulators, namely BTS, PYE and the four clade Ib bHLH. Last, we found that the over accumulation of manganese (Mn) in response to Fe shortage was reduced under combined Fe and S deficiencies. These data suggest that S deficiency inhibits the Fe deficiency dependent induction of the Fe uptake machinery. This in turn limits the transport into the root and the plant body of potentially toxic divalent cations such as Mn and Zn, thus limiting the deleterious effect of Fe deprivation.