Ferritin regulation upon ETS-4/SPDEF depletion promotes cold survival in C. elegans
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ABSTRACT:
PROVIDER: PRJNA545147 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR9137770.fastq.gz | Fastqsanger.gz | |||
| SRR9137780.fastq.gz | Fastqsanger.gz | |||
| SRR9137771.fastq.gz | Fastqsanger.gz | |||
| SRR9137781.fastq.gz | Fastqsanger.gz | |||
| SRR9137772.fastq.gz | Fastqsanger.gz |
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Project description:In this study, we subjected wild type worms and worms deficient in ETS-4, ETS-4 and DAF16, ETS-4 and PQM-1, to cold treatment and analyzed their transcriptional profiles by RNAseq.
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Project description:How animals rewire cellular programs to survive cold is a fascinating problem with potential biomedical implications, ranging from emergency medicine to space travel. Studying a hibernation-like response in the free-living nematode Caenorhabditis elegans, we uncovered a regulatory axis that enhances the natural resistance of nematodes to severe cold. This axis involves conserved transcription factors, DAF-16/FoxO and PQM-1, which jointly promote cold survival by upregulating FTN-1, a protein related to mammalian ferritin heavy chain (FTH1). Moreover, we show that inducing expression of FTH1 also promotes cold survival of mammalian neurons, a cell type particularly sensitive to deterioration in hypothermia. Our findings in both animals and cells suggest that FTN-1/FTH1 facilitates cold survival by detoxifying ROS-generating iron species. We finally show that mimicking the effects of FTN-1/FTH1 with drugs protects neurons from cold-induced degeneration, opening a potential avenue to improved treatments of hypothermia.
2022-10-14 | PXD034794 | Pride
Project description:BACKGROUND & AIMS: Stems cells within the intestinal epithelium generate daughter cells which undergo lineage commitment and maturation through the concerted action of the Wnt and Notch signalling cascades. Both pathways, in turn, regulate transcription factor networks which further define differentiation towards either enterocytes or one of three secretory cell lineages (Paneth, goblet or enteroendocrine cells). In this manuscript, we identified the Ets domain transcription factor, Spdef, as a novel lineage maker of goblet and Paneth cells. METHODS: To address the function of Spdef in vivo, we inactivated the Spdef gene and analysed the intestinal phenotype using a range of histological techniques and DNA microarray profiling. RESULTS: In accordance with the expression data we found that loss of Spdef severely impaired the maturation of goblet and Paneth cells and conversely lead to an accumulation of immature secretory progenitors. Moreover, we provide evidence suggesting that Spdef positively and negatively regulates a specific subset of goblet and Paneth cell genes including Cryptdins, Mmp7, Ang4, Kallikreins, and Muc2. CONCLUSION: We propose a model whereby Spdef acts downstream of Math1 to promote terminal differentiation of a secretory progenitor pool towards Paneth and goblet cells. Keywords: expression profiling
2010-02-10 | GSE14892 | GEO
Project description:As the list of putative driver mutations in glioma grows, we are just beginning toAs the list of putative driver mutations in glioma grows, we are just beginning to elucidate the effects of dysregulated developmental signaling pathways on the transformation of neural cells. We have employed a postnatal, mosaic, autochthonous, glioma model that captures the first hours and days of gliomagenesis in more resolution than conventional genetically engineered mouse models of cancer. We provide evidence that disruption of the Nf1-Ras pathway in the ventricular zone at multiple signaling nodes uniformly results in rapid neural stem cell depletion, progenitor hyperproliferation, and gliogenic lineage restriction. Abolishing Ets subfamily activity, which is upregulated downstream of Ras, rescues these phenotypes and blocks glioma initiation. Thus, the Nf1-Ras-Ets axis might be one of the select molecular pathways that are perturbed for initiation and maintenance in glioma. Mouse Gene 1.0 ST Microarrays from Affimetryx were used for microarray analysis. For each experiment, total RNA was fluorescently labeled and hybridized. 3 cell lines derived from in vivo electroporated neural stem and progenitors were compared.
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Project description:How ferritin regulates neutrophil leukocyte function remains unknown. To address this question, we injected mice with ferritin. bone marrow-derived neutrophils (BMDN) were isolated by density gradient centrifugation. Then we displayed RNA-seq of isolated BMDNs.
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Project description:As the list of putative driver mutations in glioma grows, we are just beginning toAs the list of putative driver mutations in glioma grows, we are just beginning to elucidate the effects of dysregulated developmental signaling pathways on the transformation of neural cells. We have employed a postnatal, mosaic, autochthonous, glioma model that captures the first hours and days of gliomagenesis in more resolution than conventional genetically engineered mouse models of cancer. We provide evidence that disruption of the Nf1-Ras pathway in the ventricular zone at multiple signaling nodes uniformly results in rapid neural stem cell depletion, progenitor hyperproliferation, and gliogenic lineage restriction. Abolishing Ets subfamily activity, which is upregulated downstream of Ras, rescues these phenotypes and blocks glioma initiation. Thus, the Nf1-Ras-Ets axis might be one of the select molecular pathways that are perturbed for initiation and maintenance in glioma.
2015-05-28 | GSE69254 | GEO
Project description:ETS-domain proteins are a family of evolutionarily conserved transcription factors (TFs) critical in the development of various cancers. Despite their recognized role in oncogenesis, the proteomic landscape of ETS family members remains underexplored. This study focuses on the systematic analysis of high-throughput proteomics data to decode the protein-protein interaction (PPI) networks and signal transduction pathways regulated by ETS factors in human cellular systems. Our findings uncover key PPIs that highlight both the redundancy and specificity of ETS family proteins, with a particular emphasis on their cooperative interactions with the MYC oncogene. These shared protein networks are strongly implicated in the pathogenesis of kidney renal clear cell carcinoma (KIRC) and other cancer types. By identifying key ETS-regulated proteins, we offer insights into novel molecular mechanisms that hold potential for therapeutic targeting. This proteomics-based approach enhances our understanding of ETS family proteins' regulatory roles, laying the groundwork for future research into oncogenic pathways and their implications in clinical oncology.
2024-10-15 | MSV000096095 | MassIVE
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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Project description:Deregulated expression of ETS transcription factors with oncogenic and tumor suppressor function occurs frequently in prostate cancer leading to profound alterations of the cancer transcriptome. By integrating genomic and functional studies we identified key targets of the aberrantly expressed ETS factors, ERG and ESE3. Altered expression of ETS factors led to the induction of the polycomb group protein EZH2 and silencing of the tumor suppressor Nkx3.1. Nkx3.1 was controlled by ERG and ESE3 both directly via binding to ETS binding sites in the gene promoter and indirectly via EZH2-induced histone H3K27 methylation. This may represent a general mechanism linking aberrantly expressed ETS with deregulation of epigenetic pathways and global reprogramming of the prostate epithelial cell transcriptome in prostate tumorigenesis. Keywords: prostate cancer, gene expression profiling, ETS genes In this study we show that deregulated expression of ETS factors with opposite functions is highly frequent in prostate cancer. Our study uncovers a previously unrecognized link between aberrant expression of ETS factors, deregulation of epigenetic pathways and silencing of tumor suppressor genes in prostate cancer and shows that partially distinct transcriptional programs are associated with different ETS gene expression patterns. The presence of distinct prostate cancer subgroups with different biological features may have important clinical implications and suggests that assessment of ETS expression levels might be useful to distinguish tumors with different clinical outcome.
2010-06-09 | E-GEOD-14206 | biostudies-arrayexpress