scholarly journals Iron storage capacities and associated ferritin gene expression among marine diatoms

2018 ◽  
Vol 63 (4) ◽  
pp. 1677-1691 ◽  
Author(s):  
Natalie R. Cohen ◽  
Elizabeth Mann ◽  
Brooke Stemple ◽  
Carly M. Moreno ◽  
Sara Rauschenberg ◽  
...  
Keyword(s):  
Gene Expression ◽  
Marine Diatoms ◽  
Iron Storage ◽  
Ferritin Gene

scholarly journals FTH1 Pseudogenes in Cancer and Cell Metabolism

Cells ◽  
2020 ◽  
Vol 9 (12) ◽  
pp. 2554
Author(s):  
Maddalena Di Sanzo ◽  
Barbara Quaresima ◽  
Flavia Biamonte ◽  
Camillo Palmieri ◽  
Maria Concetta Faniello
Keyword(s):  
Gene Expression ◽  
Cell Metabolism ◽  
Structural Features ◽  
Intracellular Iron ◽  
Iron Storage ◽  
Master Regulators ◽  
Detailed Classification ◽  
Ferritin Gene ◽  
Complex Regulatory Network ◽  
Iron Storage Protein

Ferritin, the principal intracellular iron-storage protein localized in the cytoplasm, nucleus, and mitochondria, plays a major role in iron metabolism. The encoding ferritin genes are members of a multigene family that includes some pseudogenes. Even though pseudogenes have been initially considered as relics of ancient genes or junk DNA devoid of function, their role in controlling gene expression in normal and transformed cells has recently been re-evaluated. Numerous studies have revealed that some pseudogenes compete with their parental gene for binding to the microRNAs (miRNAs), while others generate small interference RNAs (siRNAs) to decrease functional gene expression, and still others encode functional mutated proteins. Consequently, pseudogenes can be considered as actual master regulators of numerous biological processes. Here, we provide a detailed classification and description of the structural features of the ferritin pseudogenes known to date and review the recent evidence on their mutual interrelation within the complex regulatory network of the ferritin gene family.

Transforming growth factor β1 selectively regulates ferritin gene expression in malignant H-ras-transformed fibrosarcoma cell lines

2000 ◽  
Vol 78 (4) ◽  
pp. 527-535 ◽  
Author(s):  
James Lo ◽  
Robert AR Hurta
Keyword(s):  
Gene Expression ◽  
Cell Proliferation ◽  
Growth Factor ◽  
Malignant Transformation ◽  
Cell Lines ◽  
Transforming Growth Factor ◽  
Malignant Potential ◽  
Transformed Cells ◽  
Protein Synthesis Inhibitor ◽  
Ferritin Gene

Transforming growth factor β1 is an important growth regulator in many cell types, usually exerting a negative effect on cellular growth. Inhibition of DNA synthesis and cell proliferation is frequently lost during malignant transformation, and in some cases, tumor cell proliferation is actually stimulated by TGF-β1. The present study demonstrates a novel link between alterations in TGF-β1 regulation during malignant conversion, and the expression of ferritin, an important activity involved in a number of biological functions including iron homeostasis and cell-growth control. A series of H-ras-transformed mouse 10 T 1/2 cell lines, exhibiting increasing malignant potential, was investigated for possible TGF-β1-mediated changes in ferritin gene expression. Selective induction of gene expression was observed, since only H-ras-transformed cells with malignant potential exhibited marked elevations in ferritin gene expression, in particular, alterations in H-ferritin gene expression. The regulation of H-ferritin gene expression in response to TGF-β 1 did not involve alterations in transcription, but occurred through mechanisms of post-transcriptional stabilization of the H-ferritin mRNA. Additionally, evidence was obtained for a cycloheximide-sensitive regulator of H-ferritin gene expression, since the presence of this protein synthesis inhibitor increased H-ferritin message levels, and in combination with TGF-β1, cooperated in an additive manner to augment H-ferritin gene expression. These results show for the first time that TGF-β1 can regulate ferritin gene expression in malignant H-ras transformed cells, and suggest a mechanism for growth factor stimulation of malignant cells, in which early alterations in the control of H-ferritin gene expression are important.Key words: TGF-β1, ferritin gene expression, malignant transformation.

scholarly journals Adipose Tissue Expansion by Overfeeding Healthy Men Alters Iron Gene Expression

2018 ◽  
Vol 104 (3) ◽  
pp. 688-696 ◽  
Author(s):  
Berenice Segrestin ◽  
José Maria Moreno-Navarrete ◽  
Kevin Seyssel ◽  
Maud Alligier ◽  
Emmanuelle Meugnier ◽  
...  
Keyword(s):  
Gene Expression ◽  
Adipose Tissue ◽  
Serum Iron ◽  
Tissue Expansion ◽  
Lipid Storage ◽  
Mrna Levels ◽  
Intracellular Iron ◽  
Gene Encoding ◽  
Iron Storage ◽  
Healthy Men

Abstract Context Iron overload has been associated with greater adipose tissue (AT) depots. We retrospectively studied the potential interactions between iron and AT during an experimental overfeeding in participants without obesity. Methods Twenty-six participants (mean body mass index ± SD, 24.7 ± 3.1 kg/m2) underwent a 56-day overfeeding (+760 kcal/d). Serum iron biomarkers (ELISA), subcutaneous AT (SAT) gene expression, and abdominal AT distribution assessed by MRI were analyzed at the beginning and the end of the intervention. Results Before intervention: SAT mRNA expression of the iron transporter transferrin (Tf) was positively correlated with the expression of genes related to lipogenesis (lipin 1, ACSL1) and lipid storage (SCD). SAT expression of the ferritin light chain (FTL) gene, encoding ferritin (FT), an intracellular iron storage protein, was negatively correlated to SREBF1, a gene related to lipogenesis. Serum FT (mean, 92 ± 57 ng/mL) was negatively correlated with the expression of SAT genes linked to lipid storage (SCD, DGAT2) and to lipogenesis (SREBF1, ACSL1). After intervention: Overfeeding led to a 2.3 ± 1.3-kg weight gain. In parallel to increased expression of lipid storage–related genes (mitoNEET, SCD, DGAT2, SREBF1), SAT Tf, SLC40A1 (encoding ferroportin 1, a membrane iron export channel) and hephaestin mRNA levels increased, whereas SAT FTL mRNA decreased, suggesting increased AT iron requirement. Serum FT decreased to 67 ± 43 ng/mL. However, no significant associations between serum iron biomarkers and AT distribution or expansion were observed. Conclusion In healthy men, iron metabolism gene expression in SAT is associated with lipid storage and lipogenesis genes expression and is modulated during a 56-day overfeeding diet.

scholarly journals The Irr and RirA Proteins Participate in a Complex Regulatory Circuit and Act in Concert To Modulate Bacterioferritin Expression in Ensifer meliloti 1021

2017 ◽  
Vol 83 (16) ◽  
Author(s):  
Daniela Costa ◽  
Vanesa Amarelle ◽  
Claudio Valverde ◽  
Mark R. O'Brian ◽  
Elena Fabiano
Keyword(s):  
Gene Expression ◽  
Small Rna ◽  
Iron Homeostasis ◽  
Sufficient Conditions ◽  
Iron Storage ◽  
Content Type ◽  
Reading Frame ◽  
Regulatory Circuit ◽  
Ensifer Meliloti ◽  
Rhizobial Species

ABSTRACT In this work we found that the bfr gene of the rhizobial species Ensifer meliloti, encoding a bacterioferritin iron storage protein, is involved in iron homeostasis and the oxidative stress response. This gene is located downstream of and overlapping the smc03787 open reading frame (ORF). No well-predicted RirA or Irr boxes were found in the region immediately upstream of the bfr gene although two presumptive RirA boxes and one presumptive Irr box were present in the putative promoter of smc03787. We demonstrate that bfr gene expression is enhanced under iron-sufficient conditions and that Irr and RirA modulate this expression. The pattern of bfr gene expression as well as the response to Irr and RirA is inversely correlated to that of smc03787. Moreover, our results suggest that the small RNA SmelC759 participates in RirA- and Irr-mediated regulation of bfr expression and that additional unknown factors are involved in iron-dependent regulation. IMPORTANCE E. meliloti belongs to the Alphaproteobacteria, a group of bacteria that includes several species able to associate with eukaryotic hosts, from mammals to plants, in a symbiotic or pathogenic manner. Regulation of iron homeostasis in this group of bacteria differs from that found in the well-studied Gammaproteobacteria. In this work we analyzed the effect of rirA and irr mutations on bfr gene expression. We demonstrate the effect of an irr mutation on iron homeostasis in this bacterial genus. Moreover, results obtained indicate a complex regulatory circuit where multiple regulators, including RirA, Irr, the small RNA SmelC759, and still unknown factors, act in concert to balance bfr gene expression.

scholarly journals Genomic Profiling of Iron-Responsive Genes in Salmonella enterica Serovar Typhimurium by High-Throughput Screening of a Random Promoter Library

2003 ◽  
Vol 185 (16) ◽  
pp. 4973-4982 ◽  
Author(s):  
Jaime Bjarnason ◽  
Carolyn M. Southward ◽  
Michael G. Surette
Keyword(s):  
Gene Expression ◽  
High Throughput ◽  
Salmonella Enterica ◽  
High Throughput Screening ◽  
Expression Profiles ◽  
Transport Systems ◽  
Iron Availability ◽  
Iron Storage ◽  
Promoter Library ◽  
Serovar Typhimurium

ABSTRACT The importance of iron to bacteria is shown by the presence of numerous iron-scavenging and transport systems and by many genes whose expression is tightly regulated by iron availability. We have taken a global approach to gene expression analysis of Salmonella enterica serovar Typhimurium in response to iron by combining efficient, high-throughput methods with sensitive, luminescent reporting of gene expression using a random promoter library. Real-time expression profiles of the library were generated under low- and high-iron conditions to identify iron-regulated promoters, including a number of previously identified genes. Our results indicate that approximately 7% of the genome may be regulated directly or indirectly by iron. Further analysis of these clones using a Fur titration assay revealed three separate classes of genes; two of these classes consist of Fur-regulated genes. A third class was Fur independent and included both negatively and positively iron-responsive genes. These may reflect new iron-dependent regulons. Iron-responsive genes included iron transporters, iron storage and mobility proteins, iron-containing proteins (redox proteins, oxidoreductases, and cytochromes), transcriptional regulators, and the energy transducer tonB. By identifying a wide variety of iron-responsive genes, we extend our understanding of the global effect of iron availability on gene expression in the bacterial cell.

scholarly journals Post-transcriptional regulation of H-ferritin gene expression in human monocytic THP-1 cells by protein kinase C

1996 ◽  
Vol 319 (1) ◽  
pp. 185-189 ◽  
Author(s):  
Jong-Hwei S. PANG ◽  
Chia-Jung WU ◽  
Lee-Young CHAU
Keyword(s):  
Gene Expression ◽  
Protein Synthesis ◽  
Protein Kinase C ◽  
Protein Kinase ◽  
Human Fibroblasts ◽  
Leukaemic Cell ◽  
Protein Synthesis Inhibitor ◽  
Kinase C ◽  
Ferritin Gene ◽  
The Stability

The mRNA coding for H-ferritin was highly induced in human monocytic THP-1 cells following treatment with phorbol 12-myristate 13-acetate (PMA). The induction was detected at 3 h, reached maximal levels at 12 h, and was sustained for up to 48 h subsequent to PMA exposure. PMA-induced up-regulation of H-ferritin gene expression was also observed in other leukaemic cell lines, HL60 and U937, but not in non-leukaemic cell types, including human fibroblasts, endothelial cells and smooth muscle cells. The effect of PMA could be completely blocked by the protein kinase C inhibitor, H-7. Furthermore, treatment of THP-1 cells with bacterial phospholipase C also produced a marked increase in expression of H-ferritin mRNA, suggesting the activation of protein kinase C was responsible for the accumulation of mRNA. Nuclear run-off experiments demonstrated that PMA did not increase the transcriptional rate of the H-ferritin gene. In contrast, the half-life of the H-ferritin mRNA measured in the presence of actinomycin D was greatly prolonged in PMA-treated cells. The induction of H-ferritin mRNA by PMA required no protein synthesis. Conversely, treatment of THP-1 cells with protein synthesis inhibitor, cycloheximide, resulted in a 4–5-fold increase in H-ferritin mRNA. The increase in the stability of the H-ferritin mRNA was also observed in cells treated with cycloheximide. Taken together, these results suggest that the stability of H-ferritin mRNA in THP-1 is subjected to regulation via a protein kinase C-mediated phosphorylation on existing putative protein factor(s).

scholarly journals Helicobacter pylori Infection Induces Anemia, Depletes Serum Iron Storage, and Alters Local Iron-Related and Adult Brain Gene Expression in Male INS-GAS Mice

PLoS ONE ◽  
2015 ◽  
Vol 10 (11) ◽  
pp. e0142630 ◽  
Author(s):  
Monika Burns ◽  
Sureshkumar Muthupalani ◽  
Zhongming Ge ◽  
Timothy C. Wang ◽  
Vasudevan Bakthavatchalu ◽  
...  
Keyword(s):  
Gene Expression ◽  
Helicobacter Pylori ◽  
Serum Iron ◽  
Adult Brain ◽  
Helicobacter Pylori Infection ◽  
Iron Storage ◽  
Brain Gene Expression
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