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Query: UMLS:C0240066 (iron deficiency)
 7,156 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

AtbHLH29 of Arabidopsis, encoding a bHLH protein, reveals a high similarity to the tomato FER which is proposed as a transcriptional regulator involved in controlling the iron deficiency responses and the iron uptake in tomato. For identification of its biological functions, AtbHLH29 was introduced into the genome of the tomato FER mutant T3238fer mediated by Agrobacterium tumefaciencs. Transgenic plants were regenerated and the stable integration of AtbHLH29 into their genomes was confirmed by Southern hybridization. Molecular analysis demonstrated that expression of the exogenous AtbHLH29 of Arabidopsis in roots of the FER mutant T3238fer enabled to complement the defect functions of FER. The transgenic plants regained the ability to activate the whole iron deficiency responses and showed normal growth as the wild type under iron-limiting stress. Our transformation data demonstrate that AtbHLH29 is a functional ortholog of the tomato FER and can completely replace FER in controlling the effective iron acquisition in tomato. Except of iron, FER protein was directly or indirectly involved in manganese homeostasis due to that loss functions of FER in T3238fer resulted in strong reduction of Mn content in leaves and the defect function on Mn accumulation in leaves was complemented by expression of AtbHLH29 in the transgenic plants. Identification of the similar biological functions of FER and AtbHLH29, which isolated from two systematically wide-diverged "strategy I" plants, suggests that FER might be a universal gene presented in all strategy I plants in controlling effective iron acquisition system in roots.
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PMID:AtbHLH29 of Arabidopsis thaliana is a functional ortholog of tomato FER involved in controlling iron acquisition in strategy I plants. 1611 51

The transcription of genes involved in iron acquisition in plants is induced under iron deficiency, but our understanding of iron sensors and signals remains limited. Iron Deficiency-responsive Element-binding Factor 1 (IDEF1) and Hemerythrin motif-containing Really Interesting New Gene- and Zinc-finger proteins (HRZs)/BRUTUS (BTS) have recently emerged as candidate iron sensors because of their functions as potent regulators of iron deficiency responses and their iron-binding properties. IDEF1 is a central transcriptional regulator of graminaceous genes involved in iron uptake and utilization, predominantly during the early stages of iron deficiency. HRZs/BTS are E3 ubiquitin ligases and negative regulators of iron deficiency responses in both graminaceous and non-graminaceous plants. Rice OsHRZ1 and OsHRZ2 are also potent regulators of iron accumulation. Characterizing these putative iron sensors also provides clues to understanding the nature of iron signals, which may involve ionized iron itself, other metals, oxygen, redox status, heme and iron-sulfur clusters, in addition to metabolites affected by iron deficiency. Systemic iron responses may also be regulated by phloem-mobile iron and its chelators such as nicotianamine. Iron sensors and signals will be identified by demonstration of signal transmission by IDEF1, HRZs/BTS, or unknown factors.
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PMID:Iron sensors and signals in response to iron deficiency. 2490 4

Iron is an essential cofactor in numerous cellular processes. The iron deficiency in the oceans affects the primary productivity of phytoplankton including cyanobacteria. In this study, we examined the function of PfsR, a TetR family transcriptional regulator, in iron homeostasis of the cyanobacterium Synechocystis PCC 6803. Compared with the wild type, the pfsR deletion mutant displayed stronger tolerance to iron limitation and accumulated significantly more chlorophyll a, carotenoid, and phycocyanin under iron-limiting conditions. The mutant also maintained more photosystem I and photosystem II complexes than the wild type after iron deprivation. In addition, the activities of photosystem I and photosystem II were much higher in pfsR deletion mutant than in wild-type cells under iron-limiting conditions. The transcripts of pfsR were enhanced by iron limitation and inactivation of the gene affected pronouncedly expression of fut genes (encoding a ferric iron transporter), feoB (encoding a ferrous iron transporter), bfr genes (encoding bacterioferritins), ho genes (encoding heme oxygenases), isiA (encoding a chlorophyll-binding protein), and furA (encoding a ferric uptake regulator). The iron quota in pfsR deletion mutant cells was higher than in wild-type cells both before and after exposure to iron limitation. Electrophoretic mobility shift assays showed that PfsR bound to its own promoter and thereby auto-regulated its own expression. These data suggest that PfsR is a critical regulator of iron homeostasis.
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PMID:PfsR is a key regulator of iron homeostasis in Synechocystis PCC 6803. 2501 Jul 95

Using similarity search we identified Candida (Pichia) guilliermondii genes involved in iron acquisition. This yeast possesses at least four genes potentially coding for ferri-reductases, four genes encoding iron permeases and two genes codingforferroxidases. Identified C.(P.) guilliermondii genes encoding ferroxidases possess different patterns of expression under iron repletion conditions whereas their expression is activated under iron deficiency conditions or in mutant strains defective in regulation of iron acquisition. C.(P.) guilliermondii has no homologue of Saccharomyces cerevisiae transcriptional regulator of iron metabolism, Aft1p and possess an iron regulatory network similar to that of Candida albicans. Since most of C.(P.) guilliermondii known strains are not pathogenic, in contrast to that of C. albicans, we propose C.(P.) guilliermondii as safe and useful model for studying iron-dependent regulation of metabolism in yeasts belonging to CUG clade.
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PMID:PUTATIVE FERROXIDASES IN THE FLAVINOGENIC YEAST PICHIA GUILLIERMONDII ARE REGULATED BY IRON ACQUISITION. 2663 92

One of the goals of biofortification is to generate iron-enriched crops to combat growth and developmental defects especially iron (Fe) deficiency anaemia. Fe-fortification of food is challenging because soluble Fe is unstable and insoluble Fe is nonbioavailable. Genetic engineering is an alternative approach for Fe-biofortification, but so far strategies to increase Fe content have only encompassed a few genes with limited success. In this study, we demonstrate that the ethyl methanesulfonate (EMS) mutant, iron deficiency tolerant1 (idt1), can accumulate 4-7 times higher amounts of Fe than the wild type in roots, shoots and seeds, and exhibits the metal tolerance and iron accumulation (Metina) phenotype in Arabidopsis. Fe-regulated protein stability and nuclear localisation of the upstream transcriptional regulator bHLH34 were uncovered. The C to T transition mutation resulting in substitution of alanine to valine at amino acid position 320 of bHLH34 (designated as IDT1A320V ) in a conserved motif among mono- and dicots was found to be responsible for a dominant phenotype that possesses constitutive activation of the Fe regulatory pathway. Overexpression of IDT1A320V in Arabidopsis and tobacco led to the Metina phenotype; a phenotype that has escalated specificity towards optimising Fe homeostasis and may be useful in Fe-biofortification. Knowledge of the high tolerance and accumulation of heavy metals of this mutant can aid the development of tools for phytoremediation of contaminants.
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PMID:The dual benefit of a dominant mutation in Arabidopsis IRON DEFICIENCY TOLERANT1 for iron biofortification and heavy metal phytoremediation. 3167 Dec 41