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Metal ATPases are a subfamily of P-type ATPases involved in the transport of metal cations across biological membranes. They all share an architecture featuring eight transmembrane domains in pairs of two and are found in prokaryotes as well as in a variety of Eukaryotes. In Arabidopsis thaliana, eight metal P-type ATPases have been described, four being specific to copper transport and four displaying a broader metal specificity, including zinc, cadmium, and possibly copper and calcium. So far, few efforts have been devoted to elucidating the origin and evolution of these proteins in Eukaryotes. In this work, we use large-scale phylogenetics to show that metal P-type ATPases form a homogenous group among P-type ATPases and that their specialization into either monovalent (Cu) or divalent (Zn, Cd…) metal transport stems from a gene duplication that took place early in the evolution of Life. Then, we demonstrate that the four subgroups of plant metal ATPases all have a different evolutionary origin and a specific taxonomic distribution, only one tracing back to the cyanobacterial progenitor of the chloroplast. Finally, we examine the subsequent evolution of these proteins in green plants and conclude that the genes thoroughly characterized in model organisms are often the result of lineage-specific gene duplications, which calls for caution when attempting to infer function from sequence similarity alone in non-model organisms.

This review provides a comprehensive overview of the field of metal metabolism in plants, including uptake, transport inside the plant, metabolic use, deficiency, and toxicity of essential trace metals. Abstract Many trace metals are essential micronutrients, but also potent toxins. Due to natural and anthropogenic causes, vastly different trace metal concentrations occur in various habitats, ranging from deficient to toxic levels. Therefore, one focus of plant research is on the response to trace metals in terms of uptake, transport, sequestration, speciation, physiological use, deficiency, toxicity, and detoxification. In this review, we cover most of these aspects for the essential micronutrients copper, iron, manganese, molybdenum, nickel, and zinc to provide a broader overview than found in other recent reviews, to cross-link aspects of knowledge in this very active research field that are often seen in a separated way. For example, individual processes of metal usage, deficiency, or toxicity often were not mechanistically interconnected. Therefore, this review also aims to stimulate the communication of researchers following different approaches, such as gene expression analysis, biochemistry, or biophysics of metalloproteins. Furthermore, we highlight recent insights, emphasizing data obtained under physiologically and environmentally relevant conditions.

Despite its abundance in the environment, iron is poorly bioavailable and subject to strict conservation and internal recycling by most organisms. In vertebrates, the stability of iron concentration in plasma and extracellular fluid, and the total body iron content are maintained by the interaction of the iron-regulatory peptide hormone hepcidin with its receptor and cellular iron exporter ferroportin (SLC40a1). Ferroportin exports iron from duodenal enterocytes that absorb dietary iron, from iron-recycling macrophages in the spleen and the liver, and from iron-storing hepatocytes. Hepcidin blocks iron export through ferroportin, causing hypoferremia. During iron deficiency or after hemorrhage, hepcidin decreases to allow iron delivery to plasma through ferroportin, thus promoting compensatory erythropoiesis. As a host defense mediator, hepcidin increases in response to infection and inflammation, blocking iron delivery through ferroportin to blood plasma, thus limiting iron availability to invading microbes. Genetic diseases that decrease hepcidin synthesis or disrupt hepcidin binding to ferroportin cause the iron overload disorder hereditary hemochromatosis. The opposite phenotype, iron restriction or iron deficiency, can result from genetic or inflammatory overproduction of hepcidin.

Natural processes and human activities have caused widespread background contamination with non-essential toxic elements. The uptake and accumulation of cadmium (Cd), arsenic (As), and lead (Pb) by crop plants results in chronic dietary exposure and is associated with various health risks. Current human intake levels are close to what is provisionally regarded as safe. This has recently triggered legislative actions to introduce or lower limits for toxic elements in food. Arguably, the most effective way to reduce the risk of slow poisoning is the breeding of crops with much lower accumulation of contaminants. The past years have seen tremendous progress in elucidating molecular mechanisms of toxic element transport. This was achieved in the model systems Arabidopsis thaliana and, most importantly, rice, the major source of exposure to As and Cd for a large fraction of the global population. Many components of entry and sequestration pathways have been identified. This knowledge can now be applied to engineer crops with reduced toxic element accumulation especially in edible organs. Most obvious in the case of Cd, it appears likely that subtle genetic intervention has the potential to reduce human exposure to non-essential toxic elements almost immediately. This review outlines the risks and discusses our current state of knowledge with emphasis on transgenic and gene editing approaches.

Low-molecular-weight organic acids (LMWOAs) are essential O-containing metal-binding ligands involved in maintaining metal homeostasis, various metabolic processes, and plant responses to biotic and abiotic stress. Malate, citrate, and oxalate play a crucial role in metal detoxification and transport throughout the plant. This review provides a comparative analysis of the accumulation of LMWOAs in excluders, which store metals mainly in roots, and hyperaccumulators, which accumulate metals mainly in shoots. Modern concepts of the mechanisms of LMWOA secretion by the roots of excluders and hyperaccumulators are summarized, and the formation of various metal complexes with LMWOAs in the vacuole and conducting tissues, playing an important role in the mechanisms of metal detoxification and transport, is discussed. Molecular mechanisms of transport of LMWOAs and their complexes with metals across cell membranes are reviewed. It is discussed whether different endogenous levels of LMWOAs in plants determine their metal tolerance. While playing an important role in maintaining metal homeostasis, LMWOAs apparently make a minor contribution to the mechanisms of metal hyperaccumulation, which is associated mainly with root exudates increasing metal bioavailability and enhanced xylem loading of LMWOAs. The studies of metal-binding compounds may also contribute to the development of approaches used in biofortification, phytoremediation, and phytomining.

Mineral nutrition is one of the key factors determining plant productivity. In plants, metal homeostasis is achieved through the functioning of a complex system governing metal uptake, translocation, distribution, and sequestration, leading to the maintenance of a regulated delivery of micronutrients to metal-requiring processes as well as detoxification of excess or non-essential metals. Low-molecular-weight ligands, such as nicotianamine, histidine, phytochelatins, phytosiderophores, and organic acids, play an important role in metal transport and detoxification in plants. Nicotianamine and histidine are also involved in metal hyperaccumulation, which determines the ability of some plant species to accumulate a large amount of metals in their shoots. In this review we extensively summarize and discuss the current knowledge of the main pathways for the biosynthesis of these ligands, their involvement in metal uptake, radial and long-distance transport, as well as metal influx, isolation and sequestration in plant tissues and cell compartments. It is analyzed how diverse endogenous ligand levels in plants can determine their different tolerance to metal toxic effects. This review focuses on recent advances in understanding the physiological role of these compounds in metal homeostasis, which is an essential task of modern ionomics and plant physiology. It is of key importance in studying the influence of metal deficiency or excess on various physiological processes, which is a prerequisite to the improvement of micronutrient uptake efficiency and crop productivity and to the development of a variety of applications in phytoremediation, phytomining, biofortification, and nutritional crop safety.

Hyperaccumulators are being intensely investigated. They are not only interesting in scientific context due to their \"strange\" behavior in terms of dealing with high concentrations of metals, but also because of their use in phytoremediation and phytomining, for which understanding the mechanisms of hyperaccumulation is crucial. Hyperaccumulators naturally use metal accumulation as a defense against herbivores and pathogens, and therefore deal with accumulated metals in very specific ways of complexation and compartmentation, different from non-hyperaccumulator plants and also non-hyperaccumulated metals. For example, in contrast to non-hyperaccumulators, in hyperaccumulators even the classical phytochelatin-inducing metal, cadmium, is predominantly not bound by such sulfur ligands, but only by weak oxygen ligands. This applies to all hyperaccumulated metals investigated so far, as well as hyperaccumulation of the metalloid arsenic. Stronger ligands, as they have been shown to complex metals in non-hyperaccumulators, are in hyperaccumulators used for transient binding during transport to the storage sites (e.g., nicotianamine) and possibly for export of Cu in Cd/Zn hyperaccumulators [metallothioneins (MTs)]. This confirmed that enhanced active metal transport, and not metal complexation, is the key mechanism of hyperaccumulation. Hyperaccumulators tolerate the high amount of accumulated heavy metals by sequestering them into vacuoles, usually in large storage cells of the epidermis. This is mediated by strongly elevated expression of specific transport proteins in various tissues from metal uptake in the shoots up to the storage sites in the leaf epidermis. However, this mechanism seems to be very metal specific. Non-hyperaccumulated metals in hyperaccumulators seem to be dealt with like in non-hyperaccumulator plants, i.e., detoxified by binding to strong ligands such as MTs.

The Natural Resistance-Associated Macrophage Protein (NRAMP) family consists of integral membrane transporters essential for divalent metal ion transport in plants. This study aimed to identify and characterize NRAMP genes in tomato ( Solanum lycopersicum ), performing genome-wide classification, and cis-elements analysis, revealing four SlNRAMP genes in the tomato genome. Phylogenetic analysis classified the four SlNRAMP proteins into two distinct groups, group A and group B. The encoded proteins ranged in length from 509 amino acids in SlNRAMP3 to 773 amino acids in SlNRAMP4 . The number of predicted transmembrane domains in SlNRAMPs ranged from 12 to 14. Expression analysis in 20 samples from three key developmental stages were collected for metabolic profiling and RNA-seq, revealing that group A genes, including SlNRAMP1 and SlNRAMP2 , were predominantly expressed in flowers and mature roots, while group B genes, including SlNRAMP3 and SlNRAMP4 , exhibited relatively high expression in leaves and roots, respectively. The SlEIN2 gene, previously misclassified as SlNRAMP5 , has now been reassigned to a separate category. Quantitative RT‒PCR analysis demonstrated differential regulation of SlNRAMP expression in roots under cadmium and salt stress. The results highlighted that SlNRAMP4 is critical for cadmium sensitivity, whereas SlNRAMP2 plays a role in the early detection and signaling of NaCl stress. This study provides a detailed characterization of the SlNRAMP family in tomato, advancing our understanding of their roles in metal ion homeostasis and stress responses, while serving as a valuable resource for future research.

Nicotianamine (NA) is a low-molecular-weight N-containing metal-binding ligand, whose accumulation in plant organs changes under metal deficiency or excess. Although NA biosynthesis can be induced in vivo by various metals, this non-proteinogenic amino acid is mainly involved in the detoxification and transport of iron, zinc, nickel, copper and manganese. This review summarizes the current knowledge on NA biosynthesis and its regulation, considers the mechanisms of NA secretion by plant roots, as well as the mechanisms of intracellular transport of NA and its complexes with metals, and its role in radial and long-distance metal transport. Its role in metal tolerance is also discussed. The NA contents in excluders, storing metals primarily in roots, and in hyperaccumulators, accumulating metals mainly in shoots, are compared. The available data suggest that NA plays an important role in maintaining metal homeostasis and hyperaccumulation mechanisms. The study of metal-binding compounds is of interdisciplinary significance, not only regarding their effects on metal toxicity in plants, but also in connection with the development of biofortification approaches to increase the metal contents, primarily of iron and zinc, in agricultural plants, since the deficiency of these elements in food crops seriously affects human health.

Few studies have directly addressed the question of how metals (both essential and nonessential) are transported in the circulatory system of bivalve mollusks. One potential metal‐transport protein, histidine‐rich glycoprotein (HRG), has previously been isolated and characterized from the blood plasma of the marine mussel Mytilus edulis L. The present study was undertaken to investigate the extent to which mussel HRG can bind a variety of essential and nonessential metals in vitro, using immobilized metal‐ion affinity chromatography (IMAC) and sodium dodecyl sulfate–polyacrylamide gel electrophoresis. The equilibrium metal speciation model MINTEQA2 was used to compute the amount of metal that bound to the IMAC packing material during the charging and initial wash steps. Results demonstrated that HRG can bind all seven of the metals tested (Ca, Cd, Hg, Mg, Ni, Pd, and Zn) and that HRG is the only metal‐binding protein in IMAC eluents. Because HRG‐metal binding strengths (log Ka) likely correspond with histidine–metal binding strengths, and because HRG is the predominant mussel plasma protein, the majority of each of the seven metals probably would be present in mussel blood as protein‐bound metal rather than as free metal ion. The finding that a single mussel plasma protein may be responsible for binding all these metals raises important questions about how these different metals are subsequently transferred from HRG to different tissues of the mussel, where they may exhibit tissue‐specific patterns of utilization, sequestration, elimination, and toxicity.