Fe Homeostasis Research Articles

Network Topological Analysis for the Identification of Novel Hubs in Plant Nutrition.

Network analysis is a systems biology-oriented approach based on graph theory that has been recently adopted in various fields of life sciences. Starting from mitochondrial proteomes purified from roots of Cucumis sativus plants grown under single or combined iron (Fe) and molybdenum (Mo) starvation, we reconstructed and analyzed at the topological level the protein–protein interaction (PPI) and co-expression networks. Besides formate dehydrogenase (FDH), already known to be involved in Fe and Mo nutrition, other potential mitochondrial hubs of Fe and Mo homeostasis could be identified, such as the voltage-dependent anion channel VDAC4, the beta-cyanoalanine synthase/cysteine synthase CYSC1, the aldehyde dehydrogenase ALDH2B7, and the fumaryl acetoacetate hydrolase. Network topological analysis, applied to plant proteomes profiled in different single or combined nutritional conditions, can therefore assist in identifying novel players involved in multiple homeostatic interactions.

FIT and bHLH Ib transcription factors modulate iron and copper crosstalk in Arabidopsis.

Although the crosstalk between iron (Fe) and copper (Cu) homeostasis signalling networks exists in plants, the underlined molecular mechanism remains unclear. FIT (FER-LIKE IRON DEFICIENCY-INDUCED TRANSCRIPTION FACTOR) and four bHLH Ib members (bHLH38, bHLH39, bHLH100 and bHLH101) are the key regulators of Fe homeostasis. Here, we reveal that FIT and bHLH Ib control the up-regulation of Cu-uptake genes (COPT2, FRO4 and FRO5) by Fe deficiency, and Cu is required for improving plant growth under Fe-deficiency conditions. The induction of Cu-uptake gene expression and the elevation of Cu concentration are inhibited in the fit-2 or bhlh4x (the quadruple mutant of four bHLH Ib genes) under Fe-deficiency conditions. The dual overexpression of both bHLH38 (or bHLH39) and FIT activates the expression of COPT2, FRO4 and FRO5 and increases Cu accumulation. Furthermore, bHLH Ib proteins directly bind to the promoters of COPT2, FRO4 and FRO5. Either Cu supplement or overexpression of COPT2 or FRO4 improves the growth of fit-2 under Fe-deficiency conditions. Moreover, the induction of COPT2, FRO4 and FRO5 by Fe deficiency is independent of SPL7, a central regulator of Cu-deficiency responses. This work through the link between bHLH Ib/FIT and COPT2/FRO4/FRO5 under Fe-deficiency conditions establishes a new relationship between Cu and Fe homeostasis.

Roles of subcellular metal homeostasis in crop improvement

Improvement of crop production in response to rapidly changing environmental conditions is a serious challenge facing plant breeders and biotechnologists. Iron (Fe), zinc (Zn), manganese (Mn), and copper (Cu) are essential micronutrients for plant growth and reproduction. These minerals are critical to several cellular processes including metabolism, photosynthesis, and cellular respiration. Regulating the uptake and distribution of these minerals could significantly improve plant growth and development, ultimately leading to increased crop production. Plant growth is limited by mineral deficiency, but on the other hand, excess Fe, Mn, Cu, and Zn can be toxic to plants; therefore, their uptake and distribution must be strictly regulated. Moreover, the distribution of these metals among subcellular organelles is extremely important for maintaining optimal cellular metabolism. Understanding the mechanisms controlling subcellular metal distribution and availability would enable development of crop plants that are better adapted to challenging and rapidly changing environmental conditions. Here, we describe advances in understanding of subcellular metal homeostasis, with a particular emphasis on cellular Fe homeostasis in Arabidopsis and rice, and discuss strategies for regulating cellular metabolism to improve plant production.

Histone H3 lysine4 trimethylation‐regulated GRF11 expression is essential for the iron‐deficiency response in Arabidopsis thaliana

Iron (Fe) homeostasis in plants is controlled by both transcription factors (TFs) and chromatin remodeling through histone modification. To date, few studies have reported the existence of histone modification in maintaining the Fe-deficiency response. However, the reports that do exist shed light on various histone modifications, but knowledge of the activation mark in Fe-deficiency response is lacking. By using a forward genetics approach, we identified a crucial allele for Fe-deficiency response, NON-RESPONSE TO Fe-DEFICIENCY2 (NRF2), previously described as EARLY FLOWERING8 (ELF8) associated with an activation mark on histone modification, histone H3 lysine4 trimethylation. In the nrf2-1 mutant, a point mutation at ELF8T404I , exhibits impaired expression of GENERAL REGULATORY FACTOR11 (GRF11) and downstream genes in the Fe-uptake pathway. In vivo chromatin immunoprecipitation revealed that in roots, NRF2/ELF8 is essential for the expression of GRF11 for Fe-deficiency response, whereas in shoots, NRF2/ELF8 regulates FLOWERING LOCUS C (FLC) expression for flowering time control. In summary, a key factor, NRF2/ELF8, involved in epigenetic regulation essential for both flowering time control and Fe-deficiency response is uncovered.

Phytotoxicity and Iron Homeostasis Disturbance of Bismuth on <I>IRT1</I> Promoter Knockout<i> Arabidopsis thaliana</i>

Bismuth (Bi) is used in semiconductors and water pipes as a substitute for lead. The Bi concentration in the soil has not been investigated, and there is no environmental quality standard for Bi in Japan. We previously reported Bi accumulation and phytotoxicity in Arabidopsis thaliana (A. thaliana) and Solanum lycopersicum, which were presented that Bi disturb iron (Fe) homeostasis in both plants. However, the mechanism of Bi phytotoxicity remains unclear. We examined the toxic effect of Bi for the expression of Fe-related genes in A. thaliana. The microarray analysis revealed an increase of the Fe regulation cascade including the subgroup Ib transcription factor. We tried to clear the effect to Fe homeostasis using the Iron-Regulated Transporter 1 (IRT1) promoter knockout line. Bi inhibits the root growth and lateral root development, while Bi induces Fe contents. In wild type, Fe was located in the stem cell niche (SCN) without Bi condition. Fe location in IRT1 promoter knockout line was disturbed by 2 µM Bi treatment. Moreover, the cell death in root was found in 2 µM Bi treated-roots. These results suggest that Bi disturbed the Fe homeostasis, Fe overaccumulation enhanced cell death in A. thaliana, and Bi damaged SCN in the root tip.

Cu, Fe, and Zn isotope ratios in murine Alzheimer's disease models suggest specific signatures of amyloidogenesis and tauopathy

Alzheimer’s disease (AD) is characterized by accumulation of tau and amyloid-beta in the brain, and recent evidence suggests a correlation between associated protein aggregates and trace elements, such as copper, iron, and zinc. In AD, a distorted brain redox homeostasis and complexation by amyloid-beta and hyperphosphorylated tau may alter the isotopic composition of essential mineral elements. Therefore, high-precision isotopic analysis may reveal changes in the homeostasis of these elements. We used inductively coupled plasma–mass spectrometry (ICP-MS)-based techniques to determine the total Cu, Fe, and Zn contents in the brain, as well as their isotopic compositions in both mouse brain and serum. Results for male transgenic tau (Line 66, L66) and amyloid/presenilin (5xFAD) mice were compared with those for the corresponding age- and sex-matched wild-type control mice (WT). Our data show that L66 brains showed significantly higher Fe levels than did those from the corresponding WT. Significantly less Cu, but more Zn was found in 5xFAD brains. We observed significantly lighter isotopic compositions of Fe (enrichment in the lighter isotopes) in the brain and serum of L66 mice compared with WT. For 5xFAD mice, Zn exhibited a trend toward a lighter isotopic composition in the brain and a heavier isotopic composition in serum compared with WT. Neither mouse model yielded differences in the isotopic composition of Cu. Our findings indicate significant pathology-specific alterations of Fe and Zn brain homeostasis in mouse models of AD. The associated changes in isotopic composition may serve as a marker for proteinopathies underlying AD and other types of dementia.

γ-Aminobutyric Acid Suppresses Iron Transportation from Roots to Shoots in Rice Seedlings by Inducing Aerenchyma Formation.

γ-Aminobutyric acid (GABA) is a widely distributed non-protein amino acid mediated the regulation of nitrate uptake and Al3+ tolerance in plants. However, there are few reports about the involvement of GABA in the regulation of iron (Fe) acquisition and translocation. Here, we show that GABA regulates Fe homeostasis in rice seedlings. Exogenous GABA decreased the chlorophyll concentration in leaves, with or without Fe supply. Over-expression of glutamate decarboxylase (GAD) gene, coding a crucial enzyme of GABA production, elevated endogenous GABA content and caused more leaf chlorosis than wild type (Nipponbare). GABA inhibited Fe transportation from roots to shoots and GABA application elevated the expression levels of Fe deficiency (FD)-related genes under conditions of Fe-sufficiency (FS), suggesting that GABA is a regulator of Fe translocation. Using Perls’ blue staining, we found that more ferric iron (Fe3+) was deposited in the epidermal cells of roots treated with GABA compared with control roots. Anatomic section analysis showed that GABA treatment induced more aerenchyma formation compared with the control. Aerenchyma facilitated the oxidization of soluble ferrous iron (Fe2+) into insoluble Fe3+, resulted in Fe precipitation in the epidermis, and inhibited the transportation of Fe from roots to shoots.

Comparative Transcriptome Analysis of Iron and Zinc Deficiency in Maize (Zea mays L.).

Globally, one-third of the population is affected by iron (Fe) and zinc (Zn) deficiency, which is severe in developing and underdeveloped countries where cereal-based diets predominate. The genetic biofortification approach is the most sustainable and one of the cost-effective ways to address Fe and Zn malnutrition. Maize is a major source of nutrition in sub-Saharan Africa, South Asia and Latin America. Understanding systems’ biology and the identification of genes involved in Fe and Zn homeostasis facilitate the development of Fe- and Zn-enriched maize. We conducted a genome-wide transcriptome assay in maize inbred SKV616, under –Zn, –Fe and –Fe–Zn stresses. The results revealed the differential expression of several genes related to the mugineic acid pathway, metal transporters, photosynthesis, phytohormone and carbohydrate metabolism. We report here Fe and Zn deficiency-mediated changes in the transcriptome, root length, stomatal conductance, transpiration rate and reduced rate of photosynthesis. Furthermore, the presence of multiple regulatory elements and/or the co-factor nature of Fe and Zn in enzymes indicate their association with the differential expression and opposite regulation of several key gene(s). The differentially expressed candidate genes in the present investigation would help in breeding for Fe and Zn efficient and kernel Fe- and Zn-rich maize cultivars through gene editing, transgenics and molecular breeding.

Dissection of Molecular Processes and Genetic Architecture Underlying Iron and Zinc Homeostasis for Biofortification: From Model Plants to Common Wheat.

The micronutrients iron (Fe) and zinc (Zn) are not only essential for plant survival and proliferation but are crucial for human health. Increasing Fe and Zn levels in edible parts of plants, known as biofortification, is seen a sustainable approach to alleviate micronutrient deficiency in humans. Wheat, as one of the leading staple foods worldwide, is recognized as a prioritized choice for Fe and Zn biofortification. However, to date, limited molecular and physiological mechanisms have been elucidated for Fe and Zn homeostasis in wheat. The expanding molecular understanding of Fe and Zn homeostasis in model plants is providing invaluable resources to biofortify wheat. Recent advancements in NGS (next generation sequencing) technologies coupled with improved wheat genome assembly and high-throughput genotyping platforms have initiated a revolution in resources and approaches for wheat genetic investigations and breeding. Here, we summarize molecular processes and genes involved in Fe and Zn homeostasis in the model plants Arabidopsis and rice, identify their orthologs in the wheat genome, and relate them to known wheat Fe/Zn QTL (quantitative trait locus/loci) based on physical positions. The current study provides the first inventory of the genes regulating grain Fe and Zn homeostasis in wheat, which will benefit gene discovery and breeding, and thereby accelerate the release of Fe- and Zn-enriched wheats.

Altered Expression of Mitoferrin and Frataxin, Larger Labile Iron Pool and Greater Mitochondrial DNA Damage in the Skeletal Muscle of Older Adults.

Mitochondrial dysfunction and iron (Fe) dyshomeostasis are invoked among the mechanisms contributing to muscle aging, possibly via a detrimental mitochondrial–iron feed-forward loop. We quantified the labile Fe pool, Fe isotopes, and the expression of mitochondrial Fe handling proteins in muscle biopsies obtained from young and older adults. The expression of key proteins of mitochondrial quality control (MQC) and the abundance of the mitochondrial DNA common deletion (mtDNA4977) were also assessed. An inverse association was found between total Fe and the heavier Fe isotope (56Fe), indicating an increase in labile Fe abundance in cells with greater Fe content. The highest levels of labile Fe were detected in old participants with a Short Physical Performance Battery (SPPB) score ≤ 7 (low-functioning, LF). Protein levels of mitoferrin and frataxin were, respectively, higher and lower in the LF group relative to young participants and older adults with SPPB scores ≥ 11 (high-functioning, HF). The mtDNA4977 relative abundance was greater in old than in young participants, regardless of SPPB category. Higher protein levels of Pink1 were detected in LF participants compared with young and HF groups. Finally, the ratio between lipidated and non-lipidated microtubule-associated protein 1A/1B-light chain 3 (i.e., LC3B II/I), as well as p62 protein expression was lower in old participants regardless of SPPB scores. Our findings indicate that cellular and mitochondrial Fe homeostasis is perturbed in the aged muscle (especially in LF older adults), as reflected by altered levels of mitoferrin and frataxin, which, together with MQC derangements, might contribute to loss of mtDNA stability.

289 Effects of supranutritional levels of dietary zinc oxide on zinc, copper, and iron metabolism in post-weaned pigs

Abstract This study evaluated the impact of supranutritional levels of dietary zinc oxide (ZnO) on zinc (Zn), copper (Cu), and iron (Fe) homeostasis in post-weaned pigs. One hundred twenty piglets were selected at d14 of age (5.65 ± 0.68 kg). At weaning (d21), they were fed a basal post-weaning diet (without antibiotics) supplemented (n = 40/treatment) with 100 mg/kg (low; LZn), 1000 mg/kg (medium; MZn) or 3000 mg/kg (high; HZn) of ZnO until d42. Dietary levels of Cu (130 mg/kg) and Fe (260 mg/kg) remained constant throughout the experimental period. Piglets were sacrificed at d21, d23, d35, and d42 of age (n = 10/treatment/d) for samples collection. Serum concentrations and total liver content of Zn and Cu were not different among treatments on d21 and d23 (P ≥ 0.10). For Zn, treatment effects were detected at d35 and d42 (P < 0.01) on both serum concentration and total Zn content in liver. For both parameters, values were greatest for HZn, intermediary for MZn, and lowest for LZn irrespective of ages in the two periods. For Cu, treatment effects were detected at d35 and d42 (P < 0.01) on both serum concentration and total Cu content in liver. For both parameters, values were greatest for LZn and MZn and lowest for HZn irrespective of ages. For Fe, no treatment effect was detected either on whole blood Fe concentrations (P = 0.81) or hemoglobin levels (P = 0.76). However, for total Fe content in liver, treatment effects were detected (P < 0.01). Values were greatest for LZn and lowest for HZn at d35 and d42 whereas for MZn they were intermediary at d35 and similar to LZn at d42 (P ≤ 0.01). In conclusion, supranutritional levels of dietary ZnO fed to piglets during 3 weeks post-weaning significantly impacted Zn, Cu, and Fe homeostasis. These results emphasise the potential risk of Cu deficiency as well as impairment in building body Fe reserves under long-term supranutritional supplementation of ZnO.

Evidence for a role of nitric oxide in iron homeostasis in plants.

Nitric oxide (NO), once regarded as a poisonous air pollutant, is now understood as a regulatory molecule essential for several biological functions in plants. In this review, we summarize NO generation in different plant organs and cellular compartments, and also discuss the role of NO in iron (Fe) homeostasis, particularly in Fe-deficient plants. Fe is one of the most limiting essential nutrient elements for plants. Plants often exhibit Fe deficiency symptoms despite sufficient tissue Fe concentrations. NO appears to not only up-regulate Fe uptake mechanisms but also makes Fe more bioavailable for metabolic functions. NO forms complexes with Fe, which can then be delivered into target cells/tissues. NO generated in plants can alleviate oxidative stress by regulating antioxidant defense processes, probably by improving functional Fe status and by inducing post-translational modifications in the enzymes/proteins involved in antioxidant defense responses. It is hypothesized that NO acts in cooperation with transcription factors such as bHLHs, FIT, and IRO to regulate the expression of enzymes and proteins essential for Fe homeostasis. However, further investigations are needed to disentangle the interaction of NO with intracellular target molecules that leads to enhanced internal Fe availability in plants.

Mechanisms underlying iron deficiency-induced resistance against pathogens with different lifestyles.

Iron (Fe) is a poorly available mineral nutrient which affects the outcome of many cross-kingdom interactions. In Arabidopsis thaliana, Fe starvation limits infection by necrotrophic pathogens. Here, we report that Fe deficiency also reduces disease caused by the hemi-biotrophic bacterium Pseudomonas syringae and the biotrophic oomycete Hyaloperonospora arabidopsidis, indicating that Fe deficiency-induced resistance is effective against pathogens with different lifestyles. Furthermore, we show that Fe deficiency-induced resistance is not caused by withholding Fe from the pathogen but is a plant-mediated defense response that requires activity of ethylene and salicylic acid. Because rhizobacteria-induced systemic resistance (ISR) is associated with a transient up-regulation of the Fe deficiency response, we tested whether Fe deficiency-induced resistance and ISR are similarly regulated. However, Fe deficiency-induced resistance functions independently of the ISR regulators MYB72 and BGLU42, indicating that both types of induced resistance are regulated in a different manner. Mutants opt3 and frd1, which display misregulated Fe homeostasis under Fe-sufficient conditions, show disease resistance levels comparable with those of Fe-starved wild-type plants. Our results suggest that disturbance of Fe homeostasis, through Fe starvation stress or other non-homeostatic conditions, is sufficient to prime the plant immune system for enhanced defense.

Coordinated homeostasis of essential mineral nutrients: a focus on iron.

In plants, iron (Fe) transport and homeostasis are highly regulated processes. Fe deficiency or excess dramatically limits plant and algal productivity. Interestingly, complex and unexpected interconnections between Fe and various macro- and micronutrient homeostatic networks, supposedly maintaining general ionic equilibrium and balanced nutrition, are currently being uncovered. Although these interactions have profound consequences for our understanding of Fe homeostasis and its regulation, their molecular bases and biological significance remain poorly understood. Here, we review recent knowledge gained on how Fe interacts with micronutrient (e.g. zinc, manganese) and macronutrient (e.g. sulfur, phosphate) homeostasis, and on how these interactions affect Fe uptake and trafficking. Finally, we highlight the importance of developing an improved model of how Fe signaling pathways are integrated into functional networks to control plant growth and development in response to fluctuating environments.

Reactive oxygen species coordinate the transcriptional responses to iron availability in Arabidopsis.

Reactive oxygen species play a central role in the regulation of plant responses to environmental stress. Under prolonged iron (Fe) deficiency, increased levels of hydrogen peroxide (H2O2) initiate signaling events, resulting in the attenuation of Fe acquisition through the inhibition of FER-LIKE IRON DEFICIENCY-INDUCED TRANSCRIPTION FACTOR (FIT). As this H2O2 increase occurs in a FIT-dependent manner, our aim was to understand the processes involved in maintaining H2O2 levels under prolonged Fe deficiency and the role of FIT. We identified the CAT2 gene, encoding one of the three Arabidopsis catalase isoforms, as regulated by FIT. CAT2 loss-of-function plants displayed severe susceptibility to Fe deficiency and greatly increased H2O2 levels in roots. Analysis of the Fe homeostasis transcription cascade revealed that H2O2 influences the gene expression of downstream regulators FIT, BHLH genes of group Ib, and POPEYE (PYE); however, H2O2 did not affect their upstream regulators, such as BHLH104 and ILR3. Our data shows that FIT and CAT2 participate in a regulatory loop between H2O2 and prolonged Fe deficiency.

Bacillus subtilis Modulates Its Usage of Biofilm-Bound Iron in Response to Environmental Iron Availability.

Iron (Fe) is one of the most important micronutrients for most life forms on earth. While abundant in soil, Fe bioavailability in oxic soil is very low. Under environmental conditions, bacteria need to acquire sufficient Fe to sustain growth while limiting the energy cost of siderophore synthesis. Biofilm formation might mitigate this Fe stress, since it was shown to accumulate Fe in certain Gram-negative bacteria and that this Fe could be mobilized for uptake. However, it is still unclear if, and to what extent, the amount of Fe accumulated in the biofilm can sustain growth and if the mobilization of this local Fe pool is modulated by the availability of environmental Fe (i.e., Fe outside the biofilm matrix). Here, we use a nondomesticated strain of the ubiquitous biofilm-forming soil bacterium Bacillus subtilis and stable Fe isotopes to precisely evaluate the origin of Fe during growth in the presence of tannic acid and hydroxides, used as proxies for different environmental conditions. We report that this B. subtilis strain can accumulate a large quantity of Fe in the biofilm, largely exceeding Fe associated with cells. We also report that only a fraction of biofilm-bound Fe is available for uptake in the absence of other sources of Fe in the vicinity of the biofilm. We observed that the availability of environmental Fe modulates the usage of this pool of biofilm-bound Fe. Finally, our data suggest that consumption of biofilm-bound Fe relates to the efficacy of B. subtilis to transport Fe from the environment to the biofilm, possibly through siderophores.IMPORTANCE Recent pieces of evidence suggest that Fe bound to the biofilm could assume at least two important functions, a local source of Fe for uptake and a support to extracellular metabolism, such as extracellular electron transfer. Our results show that B. subtilis can use biofilm-bound Fe for uptake only if it does not compromise Fe homeostasis of the biofilm, i.e., maintains a minimum Fe concentration in the biofilm for extracellular purposes. We propose a theoretical framework based on our results and recent literature to explain how B. subtilis manages biofilm-bound Fe and Fe uptake in response to environmental Fe availability. These results provide important insights into the management of biofilm-bound and environmental Fe by B. subtilis in response to Fe stress.

QTL and candidate gene analyses of rootstock-mediated mandarin fruit yield and quality traits under contrasting iron availabilities

The most sustainable approach to overcome iron deficiency in fruit crops is breeding for rootstocks with a higher capability to acquire iron (Fe) from the soil. The objective of this study was quantitative trait loci (QTL) and candidate gene analyses of rootstock-mediated low-Fe tolerance in terms of fruit yield and quality traits, including Fe fruit content, in a satsuma mandarin-grafted rootstock population derived from a cross between Citrus reshni (Cleopatra mandarin) and Poncirus trifoliata, under sufficient and low-Fe fertilization (15.3 vs 5.2 μM Fe, respectively). Iron reduction to one-third significantly decreased satsuma leaf chlorophyll concentration, fruit iron concentration, and the fruit/leaf iron proportion. Thirty-four QTLs were detected for 46 heritable traits. Eighteen of them were also found significant when testing each parental genome separately. Seven QTLs contributed to the fruit concentrations of Cu, Fe, K, Na, and S. QTLs involved in rootstock mediated tolerance to Fe deficiency and fruit quality traits distributed into five genomic regions whose gene contents (assuming collinearity with the C. clementina genome) were investigated for overrepresented molecular functions and biological processes, and putative functional candidates. Among them, a metal-NA-transporter YSL3 (Ciclev 10019170m), four phytochelatin synthases, an iron-chelate-transporter ATPase, and four basic/helix-loop helix genes coding for likely relevant transcription factors in Fe homeostasis under Fe deficiency were found as follows: bHLH3 (Ciclev10019816m), bHLH137.1 (Ciclev10031873m), bHLH123 (Ciclev10008228m), and ILR3 (Ciclev10009354m). Genes within three QTL regions supported a genetic connection between rootstock-mediated tolerance to Fe deficiency and biotic stresses in citrus.

Arabidopsis thaliana transcription factors MYB28 and MYB29 shape ammonium stress responses by regulating Fe homeostasis.

Although ammonium (NH4+ ) is a key intermediate of plant nitrogen metabolism, high concentrations of NH4+ in the soil provoke physiological disorders that lead to the development of stress symptoms. Ammonium nutrition was shown to induce the accumulation of glucosinolates (GSLs) in leaves of different Brassicaceae species. To further understand the link between ammonium nutrition and GSLs, we analysed the ammonium stress response of Arabidopsis mutants impaired in GSL metabolic pathway. We showed that the MYB28 and MYB29 double mutant (myb28myb29), which is almost deprived of aliphatic GSLs, is highly hypersensitive to ammonium nutrition. Moreover, we evidenced that the stress symptoms developed were not a consequence of the lack of aliphatic GSLs. Transcriptomic analysis highlighted the induction of an iron (Fe) deficiency response in myb28myb29 under ammonium nutrition. Consistently, ammonium-grown myb28myb29 plants showed altered Fe accumulation and homeostasis. Interestingly, we showed overall that growing Arabidopsis with increased Fe availability relieved ammonium stress symptoms and that this was associated with MYB28 and MYB29 expression. Taken together, our data indicated that the control of Fe homeostasis was crucial for the Arabidopsis response to ammonium nutrition and evidenced that MYB28 and MYB29 play a role in this control.

Correlation of expressional pattern of Ubiquitin activating gene with grain Fe content in rice

Ubiquitin, ubiquitin-activating enzyme (E1), ubiquitin-conjugating enzyme (E2), ubiquitin ligases (E3) and 26S proteasome are the significant components of the ubiquitination process. The expression level of ubiquitin activating (UBA) gene was evaluated in 18 genotypes with differential grain iron (Fe) and zinc (Zn) (including landraces, high yielding and released biofortified varieties) at panicle initiation stage. The relative expression of the UBA gene was analysed with three yield checks- BPT 5204, MTU 1010 and Swarna and the highest gene expression level were found in land race Kalanamak followed by Jalpriya and Taroari Basmati.Significant positive correlation of expression of the UBA gene with grain Fe content suggests the possible role of ubiquitin activating enzymes in addition to the reported ubiquitin-conjugating and ligases in Fe homeostasis. The understanding of ubiquitination regulated nutrient transport mechanism is yet to be explored hence, more in-depth studies in future may provide better insight to understand the role of ubiquitination in nutrient homeostasis and develop better strategies for biofortification.

Whole-transcriptome sequencing (RNA-seq) study of the ZFL zebrafish liver cell line after acute exposure to Cd2+ ions

Cadmium (Cd) is a non-essential metal with no known biological function and a broad range of toxic effects in biological systems. We used whole-transcriptome sequencing (RNA-seq) to study the effects of Cd2+ toxicity in zebrafish liver cells, ZFL. The results of an RNA-Seq analysis of ZFL cells exposed to 5, 10 or 20 μM Cd2+ for 4- or 24-h. The differentially expressed genes affected by Cd2+ were analyzed by using Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis to study the regulated pathways. Cd2+ regulated the expression of genes associated with cellular Cu, Zn, and Fe homeostasis, DNA replication leading to cell cycle arrest and apoptosis, and glutathione metabolism. Cd2+ boosted up the amino acid synthesis, possibly to support the glutathione metabolism for tackling the oxidative stress generated from Cd2+. Cd2+ stimulation was similar to heat or xenobiotics, based on the responses from ZFL such as endoplasmic reticulum stress and protein folding. We linked also those finding of gene activations relating to carcinogenesis of Cd. This paper provides a comprehensive analysis of the expression profiles induced by Cd2+ exposure in ZFL cells, as well as useful insights into the specific toxic effects.