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 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 Characterization of Pit, a Streptococcus pneumoniae Iron Uptake ABC Transporter

2002 ◽  
Vol 70 (8) ◽  
pp. 4389-4398 ◽  
Author(s):  
Jeremy S. Brown ◽  
Sarah M. Gilliland ◽  
Javier Ruiz-Albert ◽  
David W. Holden
Keyword(s):  
Streptococcus Pneumoniae ◽  
Abc Transporter ◽  
Iron Uptake ◽  
Systemic Infection ◽  
Iron Chelator ◽  
Iron Deficient ◽  
Deficient Medium ◽  
Mutant Strains

ABSTRACT Bacteria frequently have multiple mechanisms for acquiring iron, an essential micronutrient, from the environment. We have identified a four-gene Streptococcus pneumoniae operon, named pit, encoding proteins with similarity to components of a putative Brachyspira hyodysenteriae iron uptake ABC transporter, Bit. An S. pneumoniae strain containing a defined mutation in pit has impaired growth in medium containing the iron chelator ethylenediamine di-o-hydroxyphenylacetic acid, reduced sensitivity to the iron-dependent antibiotic streptonigrin, and impaired virulence in a mouse model of S. pneumoniae systemic infection. Furthermore, addition of a mutation in pit to a strain containing mutations in the two previously described S. pneumoniae iron uptake ABC transporters, piu and pia, resulted in a strain with impaired growth in two types of iron-deficient medium, a high degree of resistance to streptonigrin, and a reduced rate of iron uptake. Comparison of the susceptibilities to streptonigrin of the individual pit, piu, and pia mutant strains and comparison of the growth in iron-deficient medium and virulence of single and double mutant strains suggest that pia is the dominant iron transporter during in vitro and in vivo growth.

scholarly journals Contribution of Siderophore Systems to Growth and Urinary Tract Colonization of Asymptomatic Bacteriuria Escherichia coli

2011 ◽  
Vol 80 (1) ◽  
pp. 333-344 ◽  
Author(s):  
Rebecca E. Watts ◽  
Makrina Totsika ◽  
Victoria L. Challinor ◽  
Amanda N. Mabbett ◽  
Glen C. Ulett ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Urinary Tract ◽  
Human Urine ◽  
Iron Uptake ◽  
Asymptomatic Bacteriuria ◽  
Content Type ◽  
E Coli ◽  
Siderophore Biosynthesis ◽  
Iron Deficient ◽  
Deficient Medium

ABSTRACTThe molecular mechanisms that define asymptomatic bacteriuria (ABU)Escherichia colicolonization of the human urinary tract remain to be properly elucidated. Here, we utilize ABUE. colistrain 83972 as a model to dissect the contribution of siderophores to iron acquisition, growth, fitness, and colonization of the urinary tract. We show thatE. coli83972 produces enterobactin, salmochelin, aerobactin, and yersiniabactin and examine the role of these systems using mutants defective in siderophore biosynthesis and uptake. Enterobactin and aerobactin contributed most to total siderophore activity and growth in defined iron-deficient medium. No siderophores were detected in an 83972 quadruple mutant deficient in all four siderophore biosynthesis pathways; this mutant did not grow in defined iron-deficient medium but grew in iron-limited pooled human urine due to iron uptake via the FecA ferric citrate receptor. In a mixed 1:1 growth assay with strain 83972, there was no fitness disadvantage of the 83972 quadruple biosynthetic mutant, demonstrating its capacity to act as a “cheater” and utilize siderophores produced by the wild-type strain for iron uptake. An 83972 enterobactin/salmochelin double receptor mutant was outcompeted by 83972 in human urine and the mouse urinary tract, indicating a role for catecholate receptors in urinary tract colonization.

scholarly journals Expression Patterns in Reductive Iron Assimilation and Functional Consequences during Phagocytosis of Lichtheimia corymbifera, an Emerging Cause of Mucormycosis

2021 ◽  
Vol 7 (4) ◽  
pp. 272
Author(s):  
Felicia Adelina Stanford ◽  
Nina Matthias ◽  
Zoltán Cseresnyés ◽  
Marc Thilo Figge ◽  
Mohamed I. Abdelwahab Hassan ◽  
...  
Keyword(s):  
Gene Expression ◽  
Iron Uptake ◽  
Intracellular Transport ◽  
Pathogenic Fungus ◽  
Expression Patterns ◽  
Iron Depletion ◽  
Iron Assimilation ◽  
Human Pathogenic Fungus ◽  
Hyphal Formation ◽  
Yeast Mutants

Iron is an essential micronutrient for most organisms and fungi are no exception. Iron uptake by fungi is facilitated by receptor-mediated internalization of siderophores, heme and reductive iron assimilation (RIA). The RIA employs three protein groups: (i) the ferric reductases (Fre5 proteins), (ii) the multicopper ferroxidases (Fet3) and (iii) the high-affinity iron permeases (Ftr1). Phenotyping under different iron concentrations revealed detrimental effects on spore swelling and hyphal formation under iron depletion, but yeast-like morphology under iron excess. Since access to iron is limited during pathogenesis, pathogens are placed under stress due to nutrient limitations. To combat this, gene duplication and differential gene expression of key iron uptake genes are utilized to acquire iron against the deleterious effects of iron depletion. In the genome of the human pathogenic fungus L. corymbifera, three, four and three copies were identified for FRE5, FTR1 and FET3 genes, respectively. As in other fungi, FET3 and FTR1 are syntenic and co-expressed in L. corymbifera. Expression of FRE5, FTR1 and FET3 genes is highly up-regulated during iron limitation (Fe-), but lower during iron excess (Fe+). Fe- dependent upregulation of gene expression takes place in LcFRE5 II and III, LcFTR1 I and II, as well as LcFET3 I and II suggesting a functional role in pathogenesis. The syntenic LcFTR1 I–LcFET3 I gene pair is co-expressed during germination, whereas LcFTR1 II- LcFET3 II is co-expressed during hyphal proliferation. LcFTR1 I, II and IV were overexpressed in Saccharomyces cerevisiae to represent high and moderate expression of intracellular transport of Fe3+, respectively. Challenge of macrophages with the yeast mutants revealed no obvious role for LcFTR1 I, but possible functions of LcFTR1 II and IVs in recognition by macrophages. RIA expression pattern was used for a new model of interaction between L. corymbifera and macrophages.

The mechanism of iron uptake in Bacillus subtilis

1970 ◽  
Vol 16 (12) ◽  
pp. 1285-1291 ◽  
Author(s):  
W. J. Peters ◽  
R. A. J. Warren
Keyword(s):  
Bacillus Subtilis ◽  
Phenolic Compounds ◽  
Phenolic Acids ◽  
Phenolic Acid ◽  
Iron Uptake ◽  
Hydroxamic Acids ◽  
Acid Complex ◽  
Iron Deficient ◽  
Active Transport System ◽  
Energy Dependent

A variety of phenolic compounds and hydroxamic acids reduced or prevented phenolic acid and coproporphyrin accumulation by iron-deficient cultures of Bacillus subtilis, but only if they were added to cultures with levels of iron which alone did not prevent accumulation. The compounds also increased iron uptake by iron-deficient cultures and norma) cultures. When radioactive catechol or 2,3-dihydroxybenzoic acid was used to increase iron uptake by iron-deficient cells, only very low levels of radioactivity remained associated with the cells. It is suggested that B. subtilis produces phenolic acids to solubilize iron; that other phenolic compounds or hydroxamic acids may substitute for the phenolic acids produced by B. subtilis; that the iron: phenolic acid complex does not enter the cell; and that the iron is removed from the complex at the cell surface and taken into the cell by an energy-dependent active transport system.

scholarly journals Regulation of Copper Metabolism by Nitrogen Utilization in Saccharomyces cerevisiae

2021 ◽  
Vol 7 (9) ◽  
pp. 756
Author(s):  
Suzie Kang ◽  
Hyewon Seo ◽  
Min-Gyu Lee ◽  
Cheol-Won Yun
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Iron Uptake ◽  
Nitrogen Starvation ◽  
Copper Metabolism ◽  
Nitrogen Utilization ◽  
Deletion Mutants ◽  
Uptake System ◽  
Wild Type ◽  
High Affinity ◽  
Uptake Activity

To understand the relationship between carbon or nitrogen utilization and iron homeostasis, we performed an iron uptake assay with several deletion mutants with partial defects in carbon or nitrogen metabolism. Among them, some deletion mutants defective in carbon metabolism partially and the MEP2 deletion mutant showed lower iron uptake activity than the wild type. Mep2 is known as a high-affinity ammonia transporter in Saccharomyces cerevisiae. Interestingly, we found that nitrogen starvation resulted in lower iron uptake activity than that of wild-type cells without downregulation of the genes involved in the high-affinity iron uptake system FET3/FTR1. However, the gene expression of FRE1 and CTR1 was downregulated by nitrogen starvation. The protein level of Ctr1 was also decreased by nitrogen starvation, and addition of copper to the nitrogen starvation medium partially restored iron uptake activity. However, the expression of MAC1, which is a copper-responsive transcriptional activator, was not downregulated by nitrogen starvation at the transcriptional level but was highly downregulated at the translational level. Mac1 was downregulated dramatically under nitrogen starvation, and treatment with MG132, which is an inhibitor of proteasome-dependent protein degradation, partially attenuated the downregulation of Mac1. Taken together, these results suggest that nitrogen starvation downregulates the high-affinity iron uptake system by degrading Mac1 in a proteasome-dependent manner and eventually downregulates copper metabolism.

Marginally excessive iron loading transiently blocks mucosal iron uptake in iron-deficient rats

2014 ◽  
Vol 307 (1) ◽  
pp. G89-G97 ◽  
Author(s):  
Shoko Shinoda ◽  
Shiho Yoshizawa ◽  
Eriko Nozaki ◽  
Kouki Tadai ◽  
Anna Arita
Keyword(s):  
Iron Uptake ◽  
Iron Concentration ◽  
Iron Loading ◽  
Short Acting ◽  
Excess Iron ◽  
Rapid Induction ◽  
Cellular Iron ◽  
Iron Load ◽  
Iron Deficient ◽  
Cellular Iron Uptake

Regular “mucosal block” is characterized by decreased uptake of a normal iron load 3–72 h after the administration of excess iron (generally 10 mg) to iron-deficient animals. We found that short-acting mucosal block could be induced by much lower iron concentration and much shorter induction time than previously reported, without affecting levels of gene expression. A rapid endocytic mechanism was reported to decrease intestinal iron absorption after a high iron load, but the activating iron load and the time to decreased absorption were undetermined. We assessed the effects of 30–2,000 μg iron load on iron uptake in the duodenal loop of iron-deficient and iron-sufficient rats under anesthesia. One hour later, mucosal cellular iron uptake in iron-deficient rats administered 30 μg iron was 76.1%, decreasing 25% to 50.7% in rats administered 2,000 μg iron. In contrast, iron uptake by iron-sufficient rats was 63% (range 60.3–65.5%) regardless of iron load. Duodenal mucosal iron concentration was significantly lower in iron-deficient than in iron-sufficient rats. Iron levels in portal blood were consistently higher in iron-deficient rats regardless of iron load, in contrast to the decreased iron uptake on the luminal side. Iron loading blocked mucosal uptake of marginally excess iron (1,000 μg), with a greater effect at 15 min than at 30 min. The rapid induction of short-acting mucosal block only in iron-deficient rats suggests DMT1 internalization.

scholarly journals Yeast protective response to arsenate involves the repression of the high affinity iron uptake system

2013 ◽  
Vol 1833 (5) ◽  
pp. 997-1005 ◽  
Author(s):  
Liliana Batista-Nascimento ◽  
Michel B. Toledano ◽  
Dennis J. Thiele ◽  
Claudina Rodrigues-Pousada
Keyword(s):  
Iron Uptake ◽  
Uptake System ◽  
Protective Response ◽  
High Affinity ◽  
Iron Uptake System

scholarly journals Insights into the chemistry of the amphibactin–metal (M3+) interaction and its role in antibiotic resistance

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Vidya Kaipanchery ◽  
Anamika Sharma ◽  
Fernando Albericio ◽  
Beatriz G. de la Torre
Keyword(s):  
Metal Ions ◽  
Iron Uptake ◽  
Pathogenic Bacteria ◽  
Iron Acquisition ◽  
Transition Metal Ions ◽  
Low Molecular Weight ◽  
Acquisition Strategies ◽  
Iron Deficient ◽  
Fe Uptake ◽  
Vibrio Genus

AbstractWe have studied the diversity and specificity of interactions of amphibactin produced by Vibrio genus bacterium (Vibrio sp. HC0601C5) with iron and various metal ions in + 3 oxidation state in an octahedral (Oh) environment. To survive in the iron-deficient environment of their host, pathogenic bacteria have devised various efficient iron acquisition strategies. One such strategy involves the production of low molecular weight peptides called siderophores, which have a strong affinity and specificity to chelate Fe3+ and can thus facilitate uptake of this metal in order to ensure iron requirements. The Fe uptake by amphibactin and the release of iron inside the cell have been studied. Comparison of the interaction of different transition metal ions (M3+) with amphibactin has been studied and it reveals that Co and Ga form stable complexes with this siderophore. The competition of Co and Ga with Fe impedes iron uptake by bacteria, thereby preventing infection.

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