Ontology highlight
ABSTRACT:
PROVIDER: PRJNA550184 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR9417750.fastq.gz | Fastqsanger.gz | |||
| SRR9417760.fastq.gz | Fastqsanger.gz | |||
| SRR9417751.fastq.gz | Fastqsanger.gz | |||
| SRR9417761.fastq.gz | Fastqsanger.gz | |||
| SRR9417752.fastq.gz | Fastqsanger.gz |
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Project description:Iron is an essential trace element whose absorption is usually tightly regulated in the duodenum. HFE-related hereditary hemochromatosis (HH) is characterized by abnormally low expression of the iron-regulatory hormone, hepcidin, which results in increased iron absorption. The liver is crucial for iron homeostasis as it is the main production site of hepcidin. The aim of this study was to explore and compare the genome-wide transcriptome response to Hfe deficiency and dietary iron overload in murine liver and duodenum.
2009-09-05 | GSE17969 | GEO
Project description:G. sulfurreducens was cultured on a variety of different iron concentrations and differential expression analysis was used to identify the iron stimulon. Wild type G. sulfurreducens was cultured on fresh water media with trace concentrations of iron (iron sufficient condition) as well as no trace iron (iron deficient condition). It was also cultured in ferric citrate (iron excess condition) media
2014-03-10 | E-GEOD-54304 | biostudies-arrayexpress
Project description:Iron is an irreplaceable co-factor for metabolism. Iron deficiency affects >1 billion people and decreased iron availability impairs immunity. Nevertheless, how iron deprivation impacts immune cell function remains poorly characterised. We interrogated how physiologically low iron availability affected CD8+ T cell metabolism and function, using multi-omic and metabolic labelling approaches. Iron limitation did not substantially alter initial post-activation increases in cell size and CD25 upregulation. However, low iron profoundly stalled proliferation (without influencing cell viability), altered histone methylation status, gene expression, and disrupted mitochondrial membrane potential. Glucose and glutamine metabolism in the TCA cycle was limited and partially reversed to a reductive trajectory. Previous studies identified mitochondria-derived aspartate as crucial for proliferation of transformed cells. Surprisingly and despite aberrant TCA cycling, aspartate was increased in stalled iron deficient CD8+ T-cells but was not utilised for nucleotide synthesis, likely due to trapping within depolarised mitochondria. Exogenous aspartate markedly rescued expansion and some functions of severely iron-deficient CD8+ T-cells. Overall, iron scarcity creates a mitochondrial-located metabolic bottleneck, which is bypassed by supplying inhibited biochemical processes with aspartate. These findings reveal molecular consequences of iron deficiency for CD8+ T cell function, providing mechanistic insight into the basis for immune impairment during iron deficiency.
2025-04-04 | MSV000097525 | MassIVE
Project description:Iron is an irreplaceable co-factor for metabolism. Iron deficiency affects >1 billion people and decreased iron availability impairs immunity. Nevertheless, how iron deprivation impacts immune cell function remains poorly characterised. We interrogated how physiologically low iron availability affected CD8+ T cell metabolism and function, using multi-omic and metabolic labelling approaches. Iron limitation did not substantially alter initial post-activation increases in cell size and CD25 upregulation. However, low iron profoundly stalled proliferation (without influencing cell viability), altered histone methylation status, gene expression, and disrupted mitochondrial membrane potential. Glucose and glutamine metabolism in the TCA cycle was limited and partially reversed to a reductive trajectory. Previous studies identified mitochondria-derived aspartate as crucial for proliferation of transformed cells. Surprisingly and despite aberrant TCA cycling, aspartate was increased in stalled iron deficient CD8+ T-cells but was not utilised for nucleotide synthesis, likely due to trapping within depolarised mitochondria. Exogenous aspartate markedly rescued expansion and some functions of severely iron-deficient CD8+ T-cells. Overall, iron scarcity creates a mitochondrial-located metabolic bottleneck, which is bypassed by supplying inhibited biochemical processes with aspartate. These findings reveal molecular consequences of iron deficiency for CD8+ T cell function, providing mechanistic insight into the basis for immune impairment during iron deficiency.
2025-04-04 | MSV000097528 | MassIVE
Project description:Iron is an irreplaceable co-factor for metabolism. Iron deficiency affects >1 billion people and decreased iron availability impairs immunity. Nevertheless, how iron deprivation impacts immune cell function remains poorly characterised. We interrogated how physiologically low iron availability affected CD8+ T cell metabolism and function, using multi-omic and metabolic labelling approaches. Iron limitation did not substantially alter initial post-activation increases in cell size and CD25 upregulation. However, low iron profoundly stalled proliferation (without influencing cell viability), altered histone methylation status, gene expression, and disrupted mitochondrial membrane potential. Glucose and glutamine metabolism in the TCA cycle was limited and partially reversed to a reductive trajectory. Previous studies identified mitochondria-derived aspartate as crucial for proliferation of transformed cells. Surprisingly and despite aberrant TCA cycling, aspartate was increased in stalled iron deficient CD8+ T-cells but was not utilised for nucleotide synthesis, likely due to trapping within depolarised mitochondria. Exogenous aspartate markedly rescued expansion and some functions of severely iron-deficient CD8+ T-cells. Overall, iron scarcity creates a mitochondrial-located metabolic bottleneck, which is bypassed by supplying inhibited biochemical processes with aspartate. These findings reveal molecular consequences of iron deficiency for CD8+ T cell function, providing mechanistic insight into the basis for immune impairment during iron deficiency.
2025-04-04 | MSV000097527 | MassIVE
Project description:Iron is an irreplaceable co-factor for metabolism. Iron deficiency affects >1 billion people and decreased iron availability impairs immunity. Nevertheless, how iron deprivation impacts immune cell function remains poorly characterised. We interrogated how physiologically low iron availability affected CD8+ T cell metabolism and function, using multi-omic and metabolic labelling approaches. Iron limitation did not substantially alter initial post-activation increases in cell size and CD25 upregulation. However, low iron profoundly stalled proliferation (without influencing cell viability), altered histone methylation status, gene expression, and disrupted mitochondrial membrane potential. Glucose and glutamine metabolism in the TCA cycle was limited and partially reversed to a reductive trajectory. Previous studies identified mitochondria-derived aspartate as crucial for proliferation of transformed cells. Surprisingly and despite aberrant TCA cycling, aspartate was increased in stalled iron deficient CD8+ T-cells but was not utilised for nucleotide synthesis, likely due to trapping within depolarised mitochondria. Exogenous aspartate markedly rescued expansion and some functions of severely iron-deficient CD8+ T-cells. Overall, iron scarcity creates a mitochondrial-located metabolic bottleneck, which is bypassed by supplying inhibited biochemical processes with aspartate. These findings reveal molecular consequences of iron deficiency for CD8+ T cell function, providing mechanistic insight into the basis for immune impairment during iron deficiency.
2025-04-04 | MSV000097526 | MassIVE
Project description:The physiology and cellular mechanisms of the dinoflagellate symbionts of cnidarians, the Symbiodiniaceae, change as a response to symbiosis, nutrient availability, and their surrounding microhabitat, but the underlying processes are poorly understood. Here, we employed liquid chromatography–mass spectrometry-based proteomics to elucidate the changes associated with the symbiotic and nutritional states of Breviolum minutum, a native symbiont of the sea anemone Exaiptasia diaphana. Both symbiosis and nutritional state had significant impacts on the B. minutum proteome. B. minutum in hospite showed increased abundance of proteins that are involved in phosphoinositol manipulation (e.g., glycerophosphoinositol permease 1 and phosphatidylinositol phosphatase), potentially as a means of interpartner signalling to prevent host phagosomal maturation. Proteins involved in carbon concentration and fixation (e.g. carbonic anhydrase, V-type ATPase) and nitrogen assimilation (e.g. glutamine synthase) were upregulated in ex hospite B. minutum, possibly due to nitrogen limitation by host in hospite and a lack of host carbon concentration mechanisms when ex hospite, respectively. Photosystem proteins increased in abundance at high nutrient levels, as were proteins involved in antioxidant mechanisms (e.g. superoxide dismutase, glutathione s-transferase). Proteins involved in iron metabolism was also affected by nutrient state, indicating increased iron demand and uptake in low nutrient treatments. These results provide better insight on the cellular mechanisms of symbiosis and provides potential target pathways for investigating a functional cnidarian-dinoflagellate symbiosis.
2023-01-31 | PXD036981 | Pride
Project description:Because iron toxicity and deficiency are equally life threatening, maintaining intracellular iron levels within a narrow optimal range is critical for nearly all known organisms. However, regulatory mechanisms that establish homeostasis are not well understood in organisms that dwell in environments at the extremes of pH, temperature, and salinity. Under conditions of limited iron, the extremophile Halobacterium salinarum, a salt-loving archaeon, mounts a specific response to scavenge iron for growth. We have identified and characterized the role of two transcription factors (TFs), Idr1 and Idr2, in regulating this important response. An integrated systems analysis of TF knockout gene expression profiles and genome-wide binding locations in the presence and absence of iron has revealed that these TFs operate collaboratively to maintain iron homeostasis. In the presence of iron, Idr1 and Idr2 bind near each other at 24 loci in the genome, where they are both required to repress some genes. In contrast, Idr1 and Idr2 are both necessary to activate other genes in a putative a feed forward loop. Even at loci bound independently, the two TFs target different genes with similar functions in iron homeostasis. We discuss conserved and unique features of the Idr1-Idr2 system in the context of similar systems in organisms from other domains of life. Data in this GEO archive are linked to the publication: Schmid AK, Pan M, Sharma K, Baliga NS.2011. Two transcription factors are necessary for iron homeostasis in a salt-dwelling archaeon.Nucleic Acids Res.39(7):2519-33. The Δura3 parent, Δidr2 and Δidr1, and Δ idr1Δidr2 mutant strains were grown to mid-logarithmic phase (OD600 ~0.4 – 0.8) in CDM with all trace metals except iron. Cultures were split in half and FeSO4 was added to one half, while the other was continued under iron limitation. 8-mL samples were collected from each culture every 20 minutes for 60 minutes (see also experimental design, Supplementary Figure 1, Schmid et al., 2011). RNA from two biological replicate time courses were prepared, averages of these replicates are reported in the published study, whereas data from each replicate are reported here. The zero time point was harvested immediately before the addition of iron. Each Sample is based on two arrrays (one with dye-swap).
2011-06-03 | E-GEOD-29704 | biostudies-arrayexpress
Project description:The fungus Candida albicans is part of the human microbiome and mainly colonises the GI tract of healthy individuals. However, when the balance in the GI tract is disturbed, the fungus can switch from a commensal to a virulent lifestyle and can turn into a life-threatening pathogen. Life in the host is characterised by a constant struggle for nutrients, essential trace elements such as iron, copper and zinc are particularly important. To protect itself from pathogens, the human host has developed a strategy to limit the availability of trace elements, this strategy is also described as nutritional immunity. C. albicans has developed a whole range of counter-strategies to obtain sufficient trace elements. In this manuscript, we have characterised the transcription factor Orf19.217, which acts at the interface between trace element scavenging and acquisition and is therefore particularly important in adaptation to life in the host. According to its identified function, we named the transcription factor Irf1, Iron-dependent Regulator of Filamentation. The transcription factor was previously identified in a systematic screen of genes whose overexpression contributes to morphological changes in C. albicans. We have comprehensively investigated the function of Irf1 using state-of-the-art functional genomics approaches, including ChIP-seq, transcriptomics and bioinformatics analyses. Analysis of the Irf1 gene-regulatory network indicates that the transcription factor is involved in the regulation of genes important for iron uptake. Using phenotypic analysis, we confirmed that Irf1 acts in a pathway parallel to known iron uptake regulators and is also required for hyphal formation induced by iron deficiency, a process that allows the fungus to access more viable body niches. Through epistasis experiments, we were also able to identify downstream effectors of Irf1 that are involved in this process. Our study provides new insights into how C. albicans adapts to iron deficiency and establish a direct functional link between hyphal formation and iron uptake.
2022-07-01 | GSE207072 | GEO