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Iron (Fe) homeostasis is essential for both plant development and human nutrition. The maintenance of Fe homeostasis involves a complex network in which Fe signaling nodes and circuits coordinate tightly Fe transporters, ferric reductases, H+ -ATPases, low-molecular-mass metal chelators, and transporters of chelators and Fe-chelate complexes. Early-stage studies have revealed different strategies for Fe homeostasis between graminaceous and nongraminaceous plants. Recent progress has refreshed our understanding of previous knowledge, especially on the uptake, phloem transport and systemic signaling of Fe. This review attempts to summarize recent exciting and potentially influential studies on the various routes of Fe uptake and distribution in plants, focusing on breakthroughs that have changed our understanding of plant Fe nutrition.

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The19th edition of the International Symposium on Iron Nutrition and Interactions in Plants, a biannual meeting initiated in 1981, took place in Taiwan for the first time. The five-day event was held at the Academia Sinica campus in the Southeast of Taiwan's capital city Taipei, and hosted around 200 scientists from around the world. The meeting covered a diverse array of topics centered around iron nutrition, including but not limited to soil processes, biofortification, transport, signaling and molecular processes regulating the cellular homeostasis of iron. Here, I review the research foci highlighted during the meeting by oral and poster presentations.

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Iron (Fe) is essential for plant growth and development. However, alkaline soils, which occupy approximately 30% of the world's arable lands, are considered Fe-limiting for plant growth because insoluble Fe (III) chelates prevail under these conditions. In contrast, high bioavailability of Fe in acidic soils can be toxic to plants due to the ability of Fe ions to promote oxidative stress. Therefore, plants have evolved sophisticated mechanisms to sense and respond to the fluctuation of Fe availability in the immediate environment and to the needs of developing shoot tissues to preclude deficiency while avoiding toxicity. In this review, we focus on recent advances in our understanding of local and systemic signaling of Fe status with emphasis on the contribution of Fe, its interaction with other metals and metal ligands in triggering molecular responses that regulate Fe uptake and partitioning in the plant body.

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Glioblastoma (GBM), the deadliest primary tumor of the central nervous system (CNS), is a clear illustration of the resistance of cancer cells to conventional therapies. Application of combinatorial strategies able to overcome pivotal factors of GBM resistance, particularly within the resection margins, represents an essential issue. This review focuses on the role of iron metabolism in GBM progression and resistance to therapy, and the impact of its pharmaceutical modulation on the disease. Iron, through its involvement in many biological processes, is a key factor in the control of cell behavior and cancer biology. Therefore, targeting cellular iron signaling or taking advantage of its dysregulation in cancer cells may lead to new opportunities for improving treatments and drug delivery in GBM.

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The paralogous iron-responsive transcription factors Aft1 and Aft2 (activators of ferrous transport) regulate iron homeostasis in Saccharomyces cerevisiae by activating expression of iron-uptake and -transport genes when intracellular iron is low. We present the previously unidentified crystal structure of Aft2 bound to DNA that reveals the mechanism of DNA recognition via specific interactions of the iron-responsive element with a Zn(2+)-containing WRKY-GCM1 domain in Aft2. We also show that two Aft2 monomers bind a [2Fe-2S] cluster (or Fe(2+)) through a Cys-Asp-Cys motif, leading to dimerization of Aft2 and decreased DNA-binding affinity. Furthermore, we demonstrate that the [2Fe-2S]-bridged heterodimer formed between glutaredoxin-3 and the BolA-like protein Fe repressor of activation-2 transfers a [2Fe-2S] cluster to Aft2 that facilitates Aft2 dimerization. Previous in vivo findings strongly support the [2Fe-2S] cluster-induced dimerization model; however, given the available evidence, Fe(2+)-induced Aft2 dimerization cannot be completely ruled out as an alternative Aft2 inhibition mechanism. Taken together, these data provide insight into the molecular mechanism for iron-dependent transcriptional regulation of Aft2 and highlight the key role of Fe-S clusters as cellular iron signals.

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