https://repository.hanyang.ac.kr/bitstream/20.500.11754/110830/1/Heavy%20metals%20in%20food%20crops%20Health%20risks%2c%20fate%2c%20mechanisms%2c%20and%20management.pdf

Heavy metals in food crops: Health risks, fate, mechanisms, and management

Heavy metal contamination of soil and water causing toxicity/stress has become one important constraint to crop productivity and quality. This situation has further worsened by the increasing population growth and inherent food demand. It have been reported in several studies that counterbalancing toxicity, due to heavy metal requires complex mechanisms at molecular, biochemical, physiological, cellular, tissue and whole plant level, which might manifest in terms of improved crop productivity. Recent advances in various disciplines of biological sciences such as metabolomics, transcriptomics, proteomics etc. have assisted in the characterization of metabolites, transcription factors, stress-inducible proteins involved in heavy metal tolerance, which in turn can be utilized for generating heavy metal tolerant crops. This review summarizes various tolerance strategies of plants under heavy metal toxicity, covering the role of metabolites (metabolomics), trace elements (ionomics), transcription factors (transcriptomics), various stress-inducible proteins (proteomics) as well as the role of plant hormones. We also provide a glance at strategies adopted by metal accumulating plants also known as “metallophytes”.

/pdf/heavy-metal-tolerance-in-plants-role-of-transcriptomics-5edq3cnn0a.pdf

Heavy Metal Tolerance in Plants: Role of Transcriptomics, Proteomics, Metabolomics, and Ionomics.

Abiotic stresses and soil nutrient limitations are major environmental conditions that reduce plant growth, productivity and quality. Plants have evolved mechanisms to perceive these environmental challenges, transmit the stress signals within cells as well as between cells and tissues, and make appropriate adjustments in their growth and development in order to survive and reproduce. In recent years, significant progress has been made on many fronts of the stress signaling research, particularly in understanding the downstream signaling events that culminate at the activation of stress- and nutrient limitation-responsive genes, cellular ion homeostasis, and growth adjustment. However, the revelation of the early events of stress signaling, particularly the identification of primary stress sensors, still lags behind. In this review, we summarize recent work on the genetic and molecular mechanisms of plant abiotic stress and nutrient limitation sensing and signaling and discuss new directions for future studies.

Plant abiotic stress response and nutrient use efficiency.

Arsenic, cadmium, lead, and mercury are toxic elements that are almost ubiquitously present at low levels in the environment because of anthropogenic influences. Dietary intake of plant-derived food represents a major fraction of potentially health-threatening human exposure, especially to arsenic and cadmium. In the interest of better food safety, it is important to reduce toxic element accumulation in crops. A molecular understanding of the pathways responsible for this accumulation can enable the development of crop varieties with strongly reduced concentrations of toxic elements in their edible parts. Such understanding is rapidly progressing for arsenic and cadmium but is in its infancy for lead and mercury. Basic discoveries have been made in Arabidopsis, rice, and other models, and most advances in crops have been made in rice. Proteins mediating the uptake of arsenic and cadmium have been identified, and the speciation and biotransformations of arsenic are now understood. Factors controlling the efficiency of root-to-shoot translocation and the partitioning of toxic elements through the rice node have also been identified.

Toxic Heavy Metal and Metalloid Accumulation in Crop Plants and Foods

Arsenic (As) and cadmium (Cd) are two toxic elements that have a relatively high risk of transfer from paddy soil to rice grain. Rice is a major dietary source of these two elements for populations consuming rice as a staple food. Reducing their accumulation in rice grain is important for food safety and human health. We review recent progress in understanding the biogeochemical processes controlling As and Cd bioavailability in paddy soil, the mechanisms of their uptake, translocation and detoxification in rice plants, and strategies to reduce their accumulation in rice grain. Similarities and differences between the two elements are emphasized. Some knowledge gaps are also identified. The concentrations of As and Cd in rice grain vary by three orders of magnitude, depending on the bioavailability of the two elements in soil, rice genotype and growing conditions. The redox potential in paddy soil has a profound but opposite effect on As and Cd bioavailability, whereas soil pH affects Cd bioavailability more than As bioavailability. A number of key genes involved in As and Cd uptake, translocation, sequestration, and detoxification in rice have been characterized. Allelic variations of several genes underlying the variations in Cd accumulation have been identified, but more remains to be elucidated, especially for As. Two types of strategies can be used to reduce As and Cd accumulation, reducing their bioavailability in soil or their uptake and translocation in rice. Reducing the accumulation of both As and Cd in rice simultaneously remains a great challenge.

/pdf/arsenic-and-cadmium-accumulation-in-rice-and-mitigation-9hejn47t27.pdf

Arsenic and cadmium accumulation in rice and mitigation strategies

Arsenic (As) is an important environmental and food-chain toxin. We investigated the key components controlling As accumulation and tolerance in Arabidopsis thaliana.
 We tested the effects of different combinations of gene knockout, including arsenate reductase (HAC1), γ-glutamyl-cysteine synthetase (γ-ECS), phytochelatin synthase (PCS1) and phosphate effluxer (PHO1), and the heterologous expression of the As-hyperaccumulator Pteris vittata arsenite efflux (PvACR3), on As tolerance, accumulation, translocation and speciation in A. thaliana.
 Heterologous expression of PvACR3 markedly increased As tolerance and root-to-shoot As translocation in A. thaliana, with PvACR3 being localized to the plasma membrane. Combining PvACR3 expression with HAC1 mutation led to As hyperaccumulation in the shoots, whereas combining HAC1 and PHO1 mutation decreased As accumulation. Mutants of γ-ECS and PCS1 were hypersensitive to As and had higher root-to-shoot As translocation. Combining γ-ECS or PCS1 with HAC1 mutation did not alter As tolerance or accumulation beyond the levels observed in the single mutants.
 PvACR3 and HAC1 have large effects on root-to-shoot As translocation. Arsenic hyperaccumulation can be engineered in A. thaliana by knocking out the HAC1 gene and expressing PvACR3. PvACR3 and HAC1 also affect As tolerance, but not to the extent of γ-ECS and PCS1.

Dissecting the components controlling root-to-shoot arsenic translocation in Arabidopsis thaliana.

The SnRK2.3-AREB1-TST1/2 cascade activated by cytosolic glucose regulates sugar accumulation across tonoplasts in apple and tomato

Inorganic arsenic is a carcinogen, and its ingestion through foods such as rice presents a significant risk to human health. Plants chemically reduce arsenate to arsenite. Using genome-wide association (GWA) mapping of loci controlling natural variation in arsenic accumulation in Arabidopsis thaliana allowed us to identify the arsenate reductase required for this reduction, which we named High Arsenic Content 1 (HAC1). Complementation verified the identity of HAC1, and expression in Escherichia coli lacking a functional arsenate reductase confirmed the arsenate reductase activity of HAC1. The HAC1 protein accumulates in the epidermis, the outer cell layer of the root, and also in the pericycle cells surrounding the central vascular tissue. Plants lacking HAC1 lose their ability to efflux arsenite from roots, leading to both increased transport of arsenic into the central vascular tissue and on into the shoot. HAC1 therefore functions to reduce arsenate to arsenite in the outer cell layer of the root, facilitating efflux of arsenic as arsenite back into the soil to limit both its accumulation in the root and transport to the shoot. Arsenate reduction by HAC1 in the pericycle may play a role in limiting arsenic loading into the xylem. Loss of HAC1-encoded arsenic reduction leads to a significant increase in arsenic accumulation in shoots, causing an increased sensitivity to arsenate toxicity. We also confirmed the previous observation that the ACR2 arsenate reductase in A. thaliana plays no detectable role in arsenic metabolism. Furthermore, ACR2 does not interact epistatically with HAC1, since arsenic metabolism in the acr2 hac1 double mutant is disrupted in an identical manner to that described for the hac1 single mutant. Our identification of HAC1 and its associated natural variation provides an important new resource for the development of low arsenic-containing food such as rice.

Genome-wide Association Mapping Identifies a New Arsenate Reductase Enzyme Critical for Limiting Arsenic Accumulation in Plants

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Dissecting the components controlling root-to-shoot arsenic translocation in Arabidopsis thaliana.

The SnRK2.3-AREB1-TST1/2 cascade activated by cytosolic glucose regulates sugar accumulation across tonoplasts in apple and tomato

Genome-wide Association Mapping Identifies a New Arsenate Reductase Enzyme Critical for Limiting Arsenic Accumulation in Plants