scholarly journals FEA1, FEA2, and FRE1, Encoding Two Homologous Secreted Proteins and a Candidate Ferrireductase, Are Expressed Coordinately with FOX1 and FTR1 in Iron-Deficient Chlamydomonas reinhardtii

2007 ◽  
Vol 6 (10) ◽  
pp. 1841-1852 ◽  
Author(s):  
Michael D. Allen ◽  
José A. del Campo ◽  
Janette Kropat ◽  
Sabeeha S. Merchant
Keyword(s):  
Iron Deficiency ◽  
Chlamydomonas Reinhardtii ◽  
Iron Uptake ◽  
Secreted Proteins ◽  
Nutrition Status ◽  
Iron Nutrition ◽  
High Affinity ◽  
Iron Deficient ◽  
Zip Family ◽  
Iron Assimilation

ABSTRACT Previously, we had identified FOX1 and FTR1 as iron deficiency-inducible components of a high-affinity copper-dependent iron uptake pathway in Chlamydomonas. In this work, we survey the version 3.0 draft genome to identify a ferrireductase, FRE1, and two ZIP family proteins, IRT1 and IRT2, as candidate ferrous transporters based on their increased expression in iron-deficient versus iron-replete cells. In a parallel proteomic approach, we identified FEA1 and FEA2 as the major proteins secreted by iron-deficient Chlamydomonas reinhardtii. The recovery of FEA1 and FEA2 from the medium of Chlamydomonas strain CC425 cultures is strictly correlated with iron nutrition status, and the accumulation of the corresponding mRNAs parallels that of the Chlamydomonas FOX1 and FTR1 mRNAs, although the magnitude of regulation is more dramatic for the FEA genes. Like the FOX1 and FTR1 genes, the FEA genes do not respond to copper, zinc, or manganese deficiency. The 5′ flanking untranscribed sequences from the FEA1, FTR1, and FOX1 genes confer iron deficiency-dependent expression of ARS2, suggesting that the iron assimilation pathway is under transcriptional control by iron nutrition. Genetic analysis suggests that the secreted proteins FEA1 and FEA2 facilitate high-affinity iron uptake, perhaps by concentrating iron in the vicinity of the cell. Homologues of FEA1 and FRE1 were identified previously as high-CO2-responsive genes, HCR1 and HCR2, in Chlorococcum littorale, suggesting that components of the iron assimilation pathway are responsive to carbon nutrition. These iron response components are placed in a proposed iron assimilation pathway for Chlamydomonas.

scholarly journals A Ferroxidase Encoded by FOX1 Contributes to Iron Assimilation under Conditions of Poor Iron Nutrition in Chlamydomonas

2008 ◽  
Vol 7 (3) ◽  
pp. 541-545 ◽  
Author(s):  
Jen-Chih Chen ◽  
Scott I. Hsieh ◽  
Janette Kropat ◽  
Sabeeha S. Merchant
Keyword(s):  
Gene Product ◽  
Iron Uptake ◽  
Iron Nutrition ◽  
Alternative Pathways ◽  
High Affinity ◽  
Iron Deficient ◽  
Zip Family ◽  
Iron Assimilation ◽  
Deficient Medium

ABSTRACT When the abundance of the FOX1 gene product is reduced, Chlamydomonas cells grow poorly in iron-deficient medium, but not in iron-replete medium, suggesting that FOX1-dependent iron uptake is a high-affinity pathway. Alternative pathways for iron assimilation, such as those involving ZIP family transporters IRT1 and IRT2, may be operational.

scholarly journals Two Iron-Responsive Promoter Elements Control Expression of FOX1 in Chlamydomonas reinhardtii

2007 ◽  
Vol 6 (11) ◽  
pp. 2163-2167 ◽  
Author(s):  
Xiaodong Deng ◽  
Mats Eriksson
Keyword(s):  
Iron Deficiency ◽  
Chlamydomonas Reinhardtii ◽  
Iron Uptake ◽  
Uptake System ◽  
Promoter Elements ◽  
High Affinity ◽  
Iron Uptake System ◽  
Iron Responsive Elements

ABSTRACT FOX1 encodes an iron deficiency-induced ferroxidase involved in a high-affinity iron uptake system. Mutagenesis analysis of the FOX1 promoter identified two separate iron-responsive elements, FeRE1 (CACACG) and FeRE2 (CACGCG), between positions −87 and −82 and between positions −65 and −60, respectively, and both are needed for induced FOX1 expression under conditions of iron deficiency.

scholarly journals nm1054: a spontaneous, recessive, hypochromic, microcytic anemia mutation in the mouse

Blood ◽  
2005 ◽  
Vol 106 (10) ◽  
pp. 3625-3631 ◽  
Author(s):  
Robert S. Ohgami ◽  
Dean R. Campagna ◽  
Brendan Antiochos ◽  
Emily B. Wood ◽  
John J. Sharp ◽  
...  
Keyword(s):  
Iron Deficiency ◽  
Iron Uptake ◽  
Genetic Locus ◽  
Failure To Thrive ◽  
Microcytic Anemia ◽  
Zinc Protoporphyrin ◽  
Hematopoietic Stem ◽  
Hypochromic Microcytic Anemia ◽  
Iron Deficient ◽  
Sparse Hair

AbstractHypochromic, microcytic anemias are typically the result of inadequate hemoglobin production because of globin defects or iron deficiency. Here, we describe the phenotypic characteristics and pathogenesis of a new recessive, hypochromic, microcytic anemia mouse mutant, nm1054. Although the mutation nm1054 is pleiotropic, also resulting in sparse hair, male infertility, failure to thrive, and hydrocephaly, the anemia is the focus of this study. Hematologic analysis reveals a moderately severe, congenital, hypochromic, microcytic anemia, with an elevated red cell zinc protoporphyrin, consistent with functional erythroid iron deficiency. However, serum and tissue iron analyses show that nm1054 animals are not systemically iron deficient. From hematopoietic stem cell transplantation and iron uptake studies in nm1054 reticulocytes, we provide evidence that the nm1054 anemia is due to an intrinsic hematopoietic defect resulting in inefficient transferrin-dependent iron uptake by erythroid precursors. Linkage studies demonstrate that nm1054 maps to a genetic locus not previously implicated in microcytic anemia or iron phenotypes.

scholarly journals Copper-Dependent Iron Assimilation Pathway in the Model Photosynthetic Eukaryote Chlamydomonas reinhardtii

2002 ◽  
Vol 1 (5) ◽  
pp. 736-757 ◽  
Author(s):  
Sharon La Fontaine ◽  
Jeanette M. Quinn ◽  
Stacie S. Nakamoto ◽  
M. Dudley Page ◽  
Vera Göhre ◽  
...  
Keyword(s):  
Iron Deficiency ◽  
Chlamydomonas Reinhardtii ◽  
Expressed Sequence Tag ◽  
Antioxidant Activities ◽  
Copper Chaperone ◽  
Iron Storage ◽  
Uptake Pathway ◽  
Unicellular Green Alga ◽  
Iron Assimilation ◽  
Sequence Relationship

ABSTRACT The unicellular green alga Chlamydomonas reinhardtii is a valuable model for studying metal metabolism in a photosynthetic background. A search of the Chlamydomonas expressed sequence tag database led to the identification of several components that form a copper-dependent iron assimilation pathway related to the high-affinity iron uptake pathway defined originally for Saccharomyces cerevisiae. They include a multicopper ferroxidase (encoded by Fox1), an iron permease (encoded by Ftr1), a copper chaperone (encoded by Atx1), and a copper-transporting ATPase. A cDNA, Fer1, encoding ferritin for iron storage also was identified. Expression analysis demonstrated that Fox1 and Ftr1 were coordinately induced by iron deficiency, as were Atx1 and Fer1, although to lesser extents. In addition, Fox1 abundance was regulated at the posttranscriptional level by copper availability. Each component exhibited sequence relationship with its yeast, mammalian, or plant counterparts to various degrees; Atx1 of C. reinhardtii is also functionally related with respect to copper chaperone and antioxidant activities. Fox1 is most highly related to the mammalian homologues hephaestin and ceruloplasmin; its occurrence and pattern of expression in Chlamydomonas indicate, for the first time, a role for copper in iron assimilation in a photosynthetic species. Nevertheless, growth of C. reinhardtii under copper- and iron-limiting conditions showed that, unlike the situation in yeast and mammals, where copper deficiency results in a secondary iron deficiency, copper-deficient Chlamydomonas cells do not exhibit symptoms of iron deficiency. We propose the existence of a copper-independent iron assimilation pathway in this organism.

scholarly journals In Vitro Bioaccessibility and Bioavailability of Iron from Mature and Microgreen Fenugreek, Rocket and Broccoli

Nutrients ◽  
2020 ◽  
Vol 12 (4) ◽  
pp. 1057
Author(s):  
Kholoud K. Khoja ◽  
Amy Buckley ◽  
Mohamad F. Aslam ◽  
Paul A. Sharp ◽  
Gladys O. Latunde-Dada
Keyword(s):  
Iron Deficiency ◽  
Iron Uptake ◽  
Mineral Content ◽  
Microwave Digestion ◽  
Surrogate Marker ◽  
Risk Groups ◽  
Ammonium Citrate ◽  
Iron Nutrition ◽  
Ferric Ammonium Citrate

Iron deficiency is a global epidemic affecting a third of the world’s population. Current efforts are focused on investigating sustainable ways to improve the bioavailability of iron in plant-based diets. Incorporating microgreens into the diet of at-risk groups in populations could be a useful tool in the management and prevention of iron deficiency. This study analysed and compared the mineral content and bioavailability of iron from microgreen and mature vegetables. The mineral content of rocket, broccoli and fenugreek microgreens and their mature counterparts was determined using microwave digestion and ICP-OES. Iron solubility and bioavailability from the vegetables were determined by a simulated gastrointestinal in vitro digestion and subsequent measurement of ferritin in Caco-2 cells as a surrogate marker of iron uptake. Iron contents of mature fenugreek and rocket were significantly higher than those of the microgreens. Mature fenugreek and broccoli showed significantly (p < 0.001) higher bioaccessibility and low-molecular-weight iron than found in the microgreens. Moreover, iron uptake by Caco-2 cells was significantly higher only from fenugreek microgreens than the mature vegetable. While all vegetables except broccoli enhanced FeSO4 uptake, the response to ferric ammonium citrate (FAC) was inhibitory apart from the mature rocket. Ascorbic acid significantly enhanced iron uptake from mature fenugreek and rocket. Microgreen fenugreek may be bred for a higher content of enhancers of iron availability as a strategy to improve iron nutrition in the populace.

scholarly journals The Adaptive Mechanism of Plants to Iron Deficiency via Iron Uptake, Transport, and Homeostasis

2019 ◽  
Vol 20 (10) ◽  
pp. 2424 ◽  
Author(s):  
Xinxin Zhang ◽  
Di Zhang ◽  
Wei Sun ◽  
Tianzuo Wang
Keyword(s):  
Iron Deficiency ◽  
Iron Uptake ◽  
Iron Homeostasis ◽  
Iron Acquisition ◽  
Essential Element ◽  
Transport Mechanisms ◽  
Iron Storage ◽  
Iron Deficient ◽  
Dicotyledonous Plants ◽  
Shed Light

Iron is an essential element for plant growth and development. While abundant in soil, the available Fe in soil is limited. In this regard, plants have evolved a series of mechanisms for efficient iron uptake, allowing plants to better adapt to iron deficient conditions. These mechanisms include iron acquisition from soil, iron transport from roots to shoots, and iron storage in cells. The mobilization of Fe in plants often occurs via chelating with phytosiderophores, citrate, nicotianamine, mugineic acid, or in the form of free iron ions. Recent work further elucidates that these genes’ response to iron deficiency are tightly controlled at transcriptional and posttranscriptional levels to maintain iron homeostasis. Moreover, increasing evidences shed light on certain factors that are identified to be interconnected and integrated to adjust iron deficiency. In this review, we highlight the molecular and physiological bases of iron acquisition from soil to plants and transport mechanisms for tolerating iron deficiency in dicotyledonous plants and rice.

scholarly journals Iron deficiency in Europe

2001 ◽  
Vol 4 (2b) ◽  
pp. 537-545 ◽  
Author(s):  
Serge Hercberg ◽  
Paul Preziosi ◽  
Pilar Galan
Keyword(s):  
Iron Deficiency ◽  
Iron Absorption ◽  
Blood Donation ◽  
Iron Status ◽  
Dietary Factors ◽  
Iron Nutrition ◽  
Dietary Recommendations ◽  
Iron Stores ◽  
Iron Deficient ◽  
Menstruating Women

AbstractIn Europe, iron deficiency is considered to be one of the main nutritional deficiency disorders affecting large fractions of the population, particularly such physiological groups as children, menstruating women and pregnant women. Some factors such as type of contraception in women, blood donation or minor pathological blood loss (haemorrhoids, gynaecological bleeding,..) considerably increase the difficulty of covering iron needs. Moreover, women, especially adolescents consuming lowenergy diets, vegetarians and vegans are at high risk of iron deficiency.Although there is no evidence that an anbsence of iron stores has any adverse consequences, it does indicate that iron nutrition is borderline, since any further reduction in body iron is associated with a decrease in the level of functional compounds such as haemoglobin.The prevalence of iron-deficient anaemia has slightly decreased in infants and menstruating women. Some positive factors may have contributed to reducing the prevalence of iron-deficiency anaemia in some groups of population: the use of iron-frotified formulas and iron-fortified cereals; the use of oral contraceptives and increased enrichment of iron in several countries; and the use of iron supplements during pregnancy in some European countries.It is possible to prevent and control iron deficiency by counseling individuals and families about sound iron nutrition during infancy and beyond, and about iron supplementation during pregnancy, by screening persons on the basis of their risk for iron deficiency, and by treating and following up persons with presumptive iron deficiency. This may help to reduce manifestations of iron deficiency and thus improve public health. Evidence linking iron status with risk of cardiovascular disease or cancer is unconvincing and does not justify changes in food fortification or medical practice, particularly because the benefits of assuring adequate iron intake during growth and development are well established. But stronger evidence is needed before rejecting the hypothesis that greater iron stores increase the incidence of CVD or cancer. At present, currently available data do not support radical changes in dietary recommendations. They include all means for increasing the content of dietary factors enhancing iron absorption or reducing the content of factors inhibiting iron absorption. Increased knowledge and increased information about factors may be important tools in the prevention of iron deficiency in Europe.

DMT1 and FPN1 expression during infancy: developmental regulation of iron absorption

2003 ◽  
Vol 285 (6) ◽  
pp. G1153-G1161 ◽  
Author(s):  
Weng-In Leong ◽  
Christopher L. Bowlus ◽  
Jonas Tallkvist ◽  
Bo Lönnerdal
Keyword(s):  
Iron Deficiency ◽  
Iron Uptake ◽  
Iron Absorption ◽  
Developmental Regulation ◽  
Total Iron ◽  
Receptor Expression ◽  
Body Iron ◽  
Rat Pups ◽  
Iron Deficient ◽  
Iron Retention

Two iron transporters, divalent metal transporter1 (DMT1) and ferroportin1 (FPN1) have been identified; however, their role during infancy is unknown. We investigated DMT1, FPN1, ferritin, and transferrin receptor expression, iron absorption and tissue iron in iron-deficient rat pups, iron-deficient rat pups given iron supplements, and controls during early ( day 10) and late infancy ( day 20). With iron deficiency, DMT1 was unchanged and FPN1 was decreased (-80%) at day 10. Body iron uptake, mucosal iron retention, and total iron absorption were unchanged. At day 20, DMT1 increased fourfold and FPN1 increased eightfold in the low-Fe group compared with controls. Body iron uptake and total iron absorption were increased, and mucosal iron retention was decreased with iron deficiency. Iron supplementation normalized expression levels of the transporters, body iron uptake, mucosal iron retention, and total iron absorption of the low-Fe group to those of controls at day 20. In summary, the molecular mechanisms regulating iron absorption during early infancy differ from late infancy when they are similar to adult animals, indicating developmental regulation of iron absorption.

Iron absorption in normal and iron-deficient beagle dogs: mucosal iron kinetics

1985 ◽  
Vol 249 (4) ◽  
pp. G439-G448 ◽  
Author(s):  
M. H. Nathanson ◽  
A. Muir ◽  
G. D. McLaren
Keyword(s):  
Iron Deficiency ◽  
Iron Deficiency Anemia ◽  
Iron Uptake ◽  
Iron Absorption ◽  
Whole Body ◽  
Deficiency Anemia ◽  
Beagle Dogs ◽  
Storage Pool ◽  
Fractional Rate ◽  
Iron Deficient

Absorption of dietary iron requires uptake of iron by the brush border of the intestinal epithelial cells, intracellular transport, and transfer to the systemic circulation. In iron-deficiency anemia, iron absorption is greatly increased, but the individual steps responsible for this increase have not been identified. We have developed a method to evaluate the rate constants for each of these steps, and we report here our results in beagle dogs a) under normal conditions and b) after phlebotomy to produce iron-deficiency anemia. Simultaneous administration of oral 59Fe3+-citrate and intravenous 55Fe-transferrin was used to investigate the kinetics of mucosal iron transport. Plasma levels of both isotopes and the whole-body excretion pattern of 59Fe were monitored sequentially, and the fractional mucosal transport rates were estimated by nonlinear least-squares fit of a physiologically based mathematical model to these data. Under normal conditions the fractional rate of mucosal iron uptake from the intestinal lumen was rate limiting, being less than 1% of the fractional rate of either iron incorporation into the mucosal storage pool or transfer of iron from the mucosa to the plasma. After induction of iron-deficiency anemia, the fractional mucosal iron uptake rate increased sixfold (P less than 0.005), while the rate of incorporation into the mucosal storage pool decreased ninefold (P less than 0.02); in contrast, the fractional rate of iron transfer to the plasma did not change. These results indicate that the enhanced iron absorption in iron-deficiency anemia is attributable to an increase in mucosal iron available for transfer to the plasma, leading in turn to a net increase in iron absorption, despite a normal fractional transfer rate.

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