Masison2022 - Cellular ferritin iron storage
Ontology highlight
ABSTRACT:
SUBMITTER: 
Pedro Mendes
PROVIDER: MODEL2211030001 | BioModels | 2023-02-07
REPOSITORIES: BioModels
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Project description:Iron-sequestration by the human host is a first line defense against respiratory pathogens like Moraxella catarrhalis, which consequently experiences a period of iron-starvation during colonization and infection. We determined the genetic requirements for M. catarrhalis growth during iron-starvation using the high-throughput genome-wide screening technology genomic array footprinting (GAF). To this end, a large marinerT7 transposon mutant library (~28,000 independent transposon mutants) was grown under iron-limiting conditions, achieved by sequestration of iron by 30 M-BM-5M Desferal (DF30), and under control growth conditions (brain heart infusion broth, DF0). Mutants were recovered at exponential- and the early-stationary growth phase and used for the generation of mutant-specific cDNA probes that were hybridized to custom-designed NimbleGen GAF microarrays. The results described in this study are further discussed in Stefan P.W. de Vries, Peter Burghout, Jeroen D. Langereis, Aldert Zomer, Peter W.M. Hermans, Hester J. Bootsma: Genetic requirements for Moraxella catarrhalis growth under iron-limiting conditions, Molecular Microbiology. cDNA probes generated from mutants recovered during the exponential growth phase, or early-stationary phase under challenge (iron-limiting, DF30) or control conditions (DF0). Hybridization on GAF 4x72K custom design Nimblegen GAF arrays for read-out.
2013-06-06 | E-GEOD-41546 | biostudies-arrayexpress
Project description:Iron-sequestration by the human host is a first line defense against respiratory pathogens like Moraxella catarrhalis, which consequently experiences a period of iron-starvation during colonization and infection. We determined the genetic requirements for M. catarrhalis growth during iron-starvation using the high-throughput genome-wide screening technology genomic array footprinting (GAF). To this end, a large marinerT7 transposon mutant library (~28,000 independent transposon mutants) was grown under iron-limiting conditions, achieved by sequestration of iron by 30 µM Desferal (DF30), and under control growth conditions (brain heart infusion broth, DF0). Mutants were recovered at exponential- and the early-stationary growth phase and used for the generation of mutant-specific cDNA probes that were hybridized to custom-designed NimbleGen GAF microarrays. The results described in this study are further discussed in Stefan P.W. de Vries, Peter Burghout, Jeroen D. Langereis, Aldert Zomer, Peter W.M. Hermans, Hester J. Bootsma: Genetic requirements for Moraxella catarrhalis growth under iron-limiting conditions, Molecular Microbiology.
2013-06-06 | GSE41546 | GEO
Project description:B. kashiwanohense PV20-2 and B. pseudolongum PV8-2 are strains isolated from breast fed iron deficient Kenyan infants, selected for their high iron sequestration mechanisms and their genome was completely sequenced. Based on their high iron sequestration features we hypothesized that B. kashiwanohense PV20-2 and B. pseudolongum PV8-2, possess iron related genes and excrete iron binding proteins in the culture media under iron limited conditions. Thus, the complete genomes of B. kashiwanohense PV20-2 and B. pseudolongum PV8-2 were compared to other bifidobacterial genomes to identify genes potentially involved in iron metabolism and the coding sequences from the genome were used as a scaffold to identify the extracellular proteome of both strains grown under low iron conditions using a gel-based shotgun proteomic approach.
2015-12-14 | PXD001451 | Pride
Project description:B. kashiwanohense PV20-2 and B. pseudolongum PV8-2 are strains isolated from breast fed iron deficient Kenyan infants, selected for their high iron sequestration mechanisms and their genome was completely sequenced. Based on their high iron sequestration features we hypothesized that B. kashiwanohense PV20-2 and B. pseudolongum PV8-2, possess iron related genes and excrete iron binding proteins in the culture media under iron limited conditions. Thus, the complete genomes of B. kashiwanohense PV20-2 and B. pseudolongum PV8-2 were compared to other bifidobacterial genomes to identify genes potentially involved in iron metabolism and the coding sequences from the genome were used as a scaffold to identify the extracellular proteome of both strains grown under low iron conditions using a gel-based shotgun proteomic approach.
2015-12-14 | PXD001452 | Pride
Project description:Iron sequestration by host iron-binding proteins is an important mechanism of resistance to microbial infections. Inside oral epithelial cells, iron is stored within the ferritin, and is therefore usually not accessible to pathogenic microbes. We observed that the ferritin concentration within oral epithelial cells was directly related to their susceptibility to damage by the human pathogenic fungus Candida albicans. Thus, we hypothesized that host ferritin may be used as an iron source by this organism. A screen of C. albicans mutants lacking components of each of the three iron acquisition systems revealed that only the reductive pathway is involved in iron utilization from ferritin by this organism. Transcriptional profiling of wild-type and hyphal-defective C. albicans strains suggested that the C. albicans invasin-like protein Als3 plays a role in ferritin binding.
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2023-08-18 | GSE241210 | GEO
Project description:Bleeding and altered iron distribution occur in multiple gastrointestinal diseases, but the significance or regulation of these changes remains unclear. Here we report that hepcidin, the master regulator of systemic iron homeostasis, is required for tissue repair in the intestine following experimental damage. This effect was independent of hepatocyte-derived hepcidin or systemic iron levels. Rather, we identified that conventional dendritic cells (DCs) are a source of hepcidin that is induced by microbial stimulation, prominent in the inflamed intestine of humans, and essential for tissue repair. Mechanistically, DC-derived hepcidin acted on ferroportin-expressing phagocytes to promote local iron sequestration, which regulated the microbiota and subsequently facilitated intestinal repair. Collectively, these results identify a novel pathway whereby DC-derived hepcidin promotes mucosal healing in the intestine via nutritional immunity.
2020-04-15 | GSE139371 | GEO
Project description:Hepatic iron overload is a risk factor for progression of hepatocellular carcinoma (HCC), although the molecular mechanisms underlying this association have remained unclear. We now show that the iron-sensing ubiquitin ligase FBXL5 is previously unrecognized oncosuppressor in liver carcinogenesis in mice. Hepatocellular iron overload evoked by FBXL5 ablation gives rise to oxidative stress, tissue damage, inflammation and compensatory proliferation in hepatocytes and to consequent promotion of liver carcinogenesis induced by exposure to a chemical carcinogen. The tumor-promoting effect of FBXL5 deficiency in the liver is also operative in a model of virus-induced HCC. FBXL5-deficient mice thus constitute the first genetically engineered mouse model of liver carcinogenesis induced by iron overload. Dysregulation of FBXL5-mediated cellular iron homeostasis was also found to be associated with poor prognosis in human HCC, implicating FBXL5 plays a significant role in defense against hepatocarcinogenesis.
2019-03-09 | GSE124370 | GEO
Project description:Iron overload in the brain, defined as excess stores of iron, is known to be related to neurological disorder. Among neurodegeneration with brain iron accumulation, we reported a specific point mutation, 977-1G>A in WDR45, showing iron accumulation in the brain, and autophagy defects in the fibroblasts. In this study, we investigated whether fibroblasts with mutated WDR45 accumulated iron, and other effects on cellular organelles. We first identified the main location of iron accumulation in the mutant fibroblasts and then investigated the effects of this accumulation on other organelles, including lipid droplets, mitochondria, and lysosomes. Ultrastructure analysis using transmission electron microscopy (TEM) and confocal microscopy showed structural changes in the organelles. Increased numbers of lipid droplets, fragmented mitochondria, and increased lysosomal vesicles with functional disorder due to WDR45 deficiency were observed. The majority of iron accumulation occurred in the lysosomal vesicles, according to correlative light and electron microscopy (CLEM). These changes were related to defects in autophagy and defective protein and organelle turnover. Gene expression profiling analysis also showed significant changes in lipid metabolism, mitochondrial function, and autophagy-related genes. Those data suggested that functional and structural changes caused impaired lipid metabolism, mitochondrial disorder, and unbalanced autophagy fluxes, due to iron overload.
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Project description:Iron accumulation in microglia has been observed in Alzheimer’s disease and other neurodegenerative disorders and is thought to contribute to disease progression through various mechanisms including neuroinflammation. To study the interaction between iron accumulation and inflammation, we treated human induced pluripotent stem cell-derived microglia (iPSC-MG) with an increasing concentration of iron, in combination with inflammatory stimuli such as interferon gamma and amyloid β, and performed RNA sequencing.
| EGAS00001006112 | EGA