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 | MSV000097526 | 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 | MSV000097525 | 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:Globally, multiple heavy metal contamination is an increasingly common problem. As heavy metals have the potential to disrupt microbially-mediated biogeochemical cycling, it is critical to understand their impact on microbial physiology. However, systems-level studies on the effects of a combination of heavy metals on bacteria are lacking. Here, we use a native Bacillus cereus isolate from the subsurface of the Oak Ridge Reservation (ORR; Oak Ridge, TN, USA) subsurface— representing a highly abundant species at the site— to assess the combined impact of eight metal contaminants. Using this metal mixture and individual metals, all at concentrations based on the ORR site geochemistry, we performed growth experiments and proteomic analyses of the B. cereus strain, in combination with targeted MS-based metabolomics and gene expression profiling. We found that the combination of eight metals impacts cell physiology in a manner that could not have been predicted from summing phenotypic responses to the individual metals. Specifically, exposure to the metal mixture elicited global iron starvation responses not observed in any of the individual metal treatments. As nitrate is also a significant contaminant at the ORR site and nitrate and nitrite reductases are iron-containing enzymes, we also examined the effects of the metal mixture on reduction of nitrogen oxides. We found that the metal mixture inhibits the activity of these enzymes through a combination of direct enzymatic damage and post-transcriptional and post-translational regulation. Altogether, these data suggest that metal mixture studies are critical for understanding how multiple rather than individual metals influence microbial processes in the environment.
2022-09-19 | PXD035730 | 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