TIM2_iron_study metagenomic assembly
Ontology highlight
ABSTRACT:
PROVIDER: PRJEB22501 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| ERR537009.fasta.gz | Fasta.gz | |||
| ERR537010.fasta.gz | Fasta.gz | |||
| ERR537006.fasta.gz | Fasta.gz |
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Project description:Gut microbial metabolism shifts towards a more toxic profile with supplementary iron in a kinetic model of the human large intestine
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Project description:Facioscapulohumeral muscular dystrophy (FSHD) is a genetic muscle disease caused by ectopic expression of the toxic protein DUX4, resulting in muscle weakness. However, the mechanism by which DUX4 exerts its toxicity remains unclear. In this study, we observed abnormal iron accumulation in muscles of patients with FSHD and in muscle-specific DUX4-expressing (DUX4-Tg) mice. Treatment with iron chelators, an iron-deficient diet, and genetic modifications inhibiting intracellular uptake of iron did not improve but rather exacerbated FSHD pathology in DUX4-Tg mice. Unexpectedly, however, iron supplementation, either from a high-iron diet or intravenous iron administration, resulted in remarkable improvement in grip strength and running performance in DUX4-Tg mice. Iron supplementation suppressed abnormal iron accumulation and the ferroptosis-related pathway involving increased lipid peroxidation in DUX4-Tg muscle. Muscle-specific DUX4 expression led to retinal vasculopathy, a part of FSHD pathology, which was prevented by iron administration. Furthermore, high-throughput compound screening of the ferroptosis pathway identified drug candidates including Ferrostatin-1 (Fer-1), a potent inhibitor of lipid peroxidation. Treatment with Fer-1 dramatically improved physical function in DUX4-Tg mice. Our findings demonstrate that DUX4-provoked toxicity is involved in the activation of the ferroptosis-related pathway and that supplementary iron could be a promising and readily available therapeutic option for FSHD.
2025-03-31 | GSE261617 | GEO
Project description:Iron is an essential metal for both animals and microbiota, and neonates and infants of humans and animals, in general, are at the risk of iron insufficient. However, excess dietary iron usually causes negative impacts on the host and microbiota. This study aimed to investigate over-loaded dietary iron supplementation on growth performance, the distribution pattern of iron in the gut lumen and the host, intestinal microbiota, and intestine gene expression profile of piglets. Sixty healthy weaning piglets were randomly assigned to six groups: fed with diets supplemented with ferrous sulfate monohydrate at the dose of 50ppm (Fe50 group), 100ppm (Fe100 group), 200ppm (Fe200 group), 500ppm (Fe500 group), and 800ppm (Fe800) for three weeks. The results indicated that increasing iron had no effects on growth performance but increased diarrheal risk and iron deposition in intestinal digesta, tissues of intestine and liver, and serum. High iron also reduced serum iron-binding capacity, apolipoprotein, and immunoglobin A. The RNA-sequencing analysis revealed that iron changed colonic gene expression profile, such as interferon gamma-signal transducer and activator of transcription 2 based anti-virus and bacteria gene network. Increasing iron also shifted cecal and colonic microbiota, such as reducing alpha diversity, Clostridiales and Lactobacillus reuteri, and increasing Lactobacillus and Lactobacillus amylovorus. Collectively, this study demonstrated that high dietary iron increased diarrheal incidence, changed intestinal immune response-associated gene expression, and shifts gut microbiota. The results would enhance our knowledge of iron effects on the gut and microbiome in piglets, and further contribute to understanding these aspects in humans.
2020-09-20 | GSE158245 | GEO
Project description:Iron chelation shifts endothelial phenotypes
| PRJNA1389469 | ENA
Project description:Serum samples were taken from four healthy donors before a meal and 3, 5, 7, 9 h after a meal (Supplementary Table S6, Sheet 1). The analysis of the serum peptidome against the HuMiProt90 database showed that the amount of non-human peptides (potentially bacterial peptides) in the bloodstream significantly increased 5 h after a meal (Figure 3D, Supplementary Table S6, Sheet 3). The comparison of these data with the transit time of food in different parts of the gastrointestinal tract suggests that bacterial peptides enter the bloodstream predominantly in the small intestine. At the same time, phyla Proteobacteria, Firmicutes and Actinobacteria are the main contributors to the increase in (potentially) bacterial peptides 5 h after a meal (Supplementary Table S6, Sheets 5 and 6).
2024-06-14 | PXD027618 | Pride
Project description:Starvation in diploid budding yeast cells triggers a cell-fate program culminating in meiosis and spore formation. Transcription activation of early meiotic genes (EMGs) hinges on the transcription activator Ime1, its DNA-binding partner Ume6, and GSK-3 kinase Rim11. Phosphorylation of Ume6 by Rim11 is key for EMG activation. We report that Rim11 functions as the central signal integrator for controlling Ume6 phosphorylation and EMG transcription. In nutrient-rich conditions, PKA suppresses Rim11 levels, while TORC1 retains Rim11 in the cytoplasm. Inhibiting PKA and TORC1 induces Rim11 expression and nuclear localization. Remarkably, nuclear Rim11 is required, but not sufficient, for Rim11-dependent Ume6 phosphorylation. Additionally, Ime1 is an essential anchor protein for phosphorylating Ume6. Subsequently, Ume6-Ime1 coactivator complexes form, which drive EMG transcription. Our results demonstrate how varied signalling inputs (PKA/TORC1/Ime1) converge through Rim11 to regulate EMG expression and meiosis initiation. We posit that the signalling-regulatory network elucidated here generates robustness in cell-fate control.
2024-03-06 | PXD049212 | Pride
Project description:Bariatric surgeries remain the most effective treatments for sustained weight loss and remission of type 2 diabetes. In addition to decreased body weight and improved glucose regulation, these procedures also dramatically increase secretion of several gut hormones including GLP-1. Despite these benefits, there are deleterious side effects to these procedures that include an increased incidence of iron-deficiency related anemias. The transcription factor HIF2a is heavily expressed in the duodenum and regulates the molecular machinery of iron absorption from the lumen. Lower iron levels after both gastric bypass and sleeve gastrectomy procedures occur despite dramatic upregulation of HIF2a signaling in the duodenum and are likely the result of increased hepcidin levels. Low iron diets also stimulate increased HIF2a signaling in the duodenum and produce effects similar to bariatric surgery that include reduced body weight/fat, improved glucose regulation and increased secretion of the GLP-1. Gut-specific deletion of VHL results in a constitutive upregulation of HIF2a signaling in the small intestine and produces a dramatic phenotype that includes reduced body weight/fat, improved glucose tolerance and increased GLP-1 secretion from the intestine. These data demonstrate an important role of HIF2a signaling in the duodenum to regulate multiple aspects of systemic metabolism and gut hormone secretion pointing towards critical cross-talk between the systems that regulate iron and other aspects of systemic physiology important to prevalent metabolic diseases.
2022-02-03 | GSE169402 | GEO
Project description:Bariatric surgeries remain the most effective treatments for sustained weight loss and remission of type 2 diabetes. In addition to decreased body weight and improved glucose regulation, these procedures also dramatically increase secretion of several gut hormones including GLP-1. Despite these benefits, there are deleterious side effects to these procedures that include an increased incidence of iron-deficiency related anemias. The transcription factor HIF2a is heavily expressed in the duodenum and regulates the molecular machinery of iron absorption from the lumen. Lower iron levels after both gastric bypass and sleeve gastrectomy procedures occur despite dramatic upregulation of HIF2a signaling in the duodenum and are likely the result of increased hepcidin levels. Low iron diets also stimulate increased HIF2a signaling in the duodenum and produce effects similar to bariatric surgery that include reduced body weight/fat, improved glucose regulation and increased secretion of the GLP-1. Gut-specific deletion of VHL results in a constitutive upregulation of HIF2a signaling in the small intestine and produces a dramatic phenotype that includes reduced body weight/fat, improved glucose tolerance and increased GLP-1 secretion from the intestine. These data demonstrate an important role of HIF2a signaling in the duodenum to regulate multiple aspects of systemic metabolism and gut hormone secretion pointing towards critical cross-talk between the systems that regulate iron and other aspects of systemic physiology important to prevalent metabolic diseases.
2022-02-03 | GSE169400 | GEO
Project description:Early meiotic genes (EMGs) encompass an important subset within the developmental program of gametogenesis. Regulation of EMGs is achieved through the recognition of a common regulatory element in their promoters by the transcription factor Ume6. Proper meiotic execution requires the timely expression of EMGs, which is achieved through the adoption of the meiotic regulator Ime1 by Ume6. While it is known that Ime1’s binding to Ume6 promotes EMG expression, the mechanism of EMG activation remains unclear. Two competing models have been proposed: (1) Ime1 converts Ume6 to a coactivator complex, and (2) Ime1 binding targets Ume6 for degradation. Using a combination of tools including meiotic synchronization, temporally controlled protein depletion, protein-protein interaction engineering, and transcriptomics, here we address this conundrum. We identify 160 genes that are directly regulated by Ime1-Ume6, including UME6 itself. Removal of Ume6 shortly before meiotic entry is detrimental to EMG activation and gamete formation, whereas tethering of Ume6 to a heterologous activation domain is sufficient to trigger EMG expression and to generate viable gametes in the absence of Ime1. We conclude that Ime1-Ume6 functions as a coactivator complex. While Ume6 is indispensable for EMGs expression, Ime1 primarily serves as an evolutionarily tuned activation domain for Ume6.
2023-06-30 | GSE226769 | GEO