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Genome-wide mapping of Hif-1α binding sites in zebrafish [microarray]

ABSTRACT: Analysis of gene expression changes in the von Hippel Lindau when mutant compared to wild-type at 4dpf using a whole genome microarray expression profiling. The von Hippel Lindau mutant displays a systemic hypoxic response under normoxic conditions. We performed single-colour microarrays to identify the gene expression changes which underpin the hypoxic phenotype. We used 3 biological replicates from both mutant and control, followed by analysis using Limma to identify significant gene expression changes. This work, together with ChIP-seq data for the Hif-1α in von Hippel Lindau mutants, should allow for the Hif-1α dependency of these gene expression changes to be assessed.

ORGANISM(S): Danio rerio

PROVIDER: GSE70885 | GEO | 2016/03/22

SECONDARY ACCESSION(S): PRJNA289856

REPOSITORIES: GEO

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Genome-wide mapping of Hif-1Î± binding sites in zebrafish [microarray]

Project description:Analysis of gene expression changes in the von Hippel Lindau when mutant compared to wild-type at 4dpf using a whole genome microarray expression profiling. The von Hippel Lindau mutant displays a systemic hypoxic response under normoxic conditions. We performed single-colour microarrays to identify the gene expression changes which underpin the hypoxic phenotype. We used 3 biological replicates from both mutant and control, followed by analysis using Limma to identify significant gene expression changes. This work, together with ChIP-seq data for the Hif-1Î± in von Hippel Lindau mutants, should allow for the Hif-1Î± dependency of these gene expression changes to be assessed. The changes in gene expression between von Hippel Lindau mutants and wild-type controls was measured at 4 days post fertilisation. For both wild-type and mutant, 3 biological replicates, each of 30 embryos were used.

2016-03-22 | E-GEOD-70885 | biostudies-arrayexpress

Genome-wide mapping of Hif-1α binding sites in zebrafish [ChIP-seq]

Project description:Analysis of the binding sites of Hif-1α in both wild-type and von Hippel Lindau mutant zebrafish lines at 4dpf by ChIP linked next generation sequencing. The von Hippel Lindau mutant displays a systemic hypoxic response under normoxic conditions. Results show the extent of Hif-1α binding to the genome, and provide a basis for analysis of the transcriptional response to genetically induced hypoxia in zebrafish.

2016-03-22 | GSE70727 | GEO

Genome-wide mapping of Hif-1Î± binding sites in zebrafish [ChIP-seq]

Project description:Analysis of the binding sites of Hif-1Î± in both wild-type and von Hippel Lindau mutant zebrafish lines at 4dpf by ChIP linked next generation sequencing. The von Hippel Lindau mutant displays a systemic hypoxic response under normoxic conditions. Results show the extent of Hif-1Î± binding to the genome, and provide a basis for analysis of the transcriptional response to genetically induced hypoxia in zebrafish. Analysis of the DNA binding sites of Hif-1Î± in both wild-type and von Hippel Lindau mutant zebrafish lines at 4dpf. The von Hippel Lindau mutant displays a systemic hypoxic response under normoxic conditions. Results show the extent of Hif-1Î± binding to the genome, and provide a basis for analysis of the dependency of the transcriptional response on Hif-1Î± in conditions of genetically induced hypoxia in zebrafish.

2016-03-22 | E-GEOD-70727 | biostudies-arrayexpress

RNA expression data from kidneys lacking von Hippel-Lindau (VHL) protein in tubular epithelial cells

2014-01-17 | GSE54172 | GEO

Transcription profiling of liver from mice with constitutively active Hypoxia Inducible Factor (HIF-1a and HIF-2a) or inactivated von Hippel-Lindau tumor suppressor gene product (pVHL)

Project description:The effects of constitutively active Hypoxia Inducible Factor (HIF) and inactivated von Hippel-Lindau tumor suppressor gene product (pVHL) were examined in a mouse model. Conditionally expressed, constitutively active HIF-1a and HIF-2a were compared with inactivated pVHL.

2006-09-21 | E-MEXP-856 | biostudies-arrayexpress

ID2 and HIF-1α Collaborate to Protect Quiescent Hematopoietic Stem Cells from Activation, Differentiation and Exhaustion [RNA-seq]

Project description:Defining mechanism(s) that maintain tissue stem quiescence is important for improving tissue regeneration, cell therapies, aging, and cancer. We report here that genetic ablation of Id2 in adult hematopoietic stem cells (HSCs) promotes increased HSC activation and differentiation, which results in HSC exhaustion and bone marrow failure over time. Id2Δ/Δ HSCs show increased HSC cycling, reactive oxygen species (ROS) production, mitochondrial activation, and DNA damage supporting the conclusion that Id2Δ/Δ HSCs are less quiescent. Mechanistically, HIF-1α expression is decreased in Id2Δ/Δ HSCs, and stabilization of HIF-1α in Id2Δ/Δ HSCs restores HSC quiescence and rescues HSC exhaustion. ID2 promotes HIF-1α expression by binding to the Von Hippel-Lindau (VHL) protein and interfering with proteasomal degradation of HIF-1α. HIF-1α promotes Id2 expression and enforces a positive feedback loop between ID2 and HIF-1α to maintain HSC quiescence. Thus, sustained ID2 expression could protect HSCs during stress, and improve HSC expansion for gene editing and cell therapies.

2022-05-31 | GSE203076 | GEO

ID2 and HIF-1α collaborate to Protect Quiescent Hematopoietic Stem Cells from Activation, Differentiation and Exhaustion [scRNA-seq]

Project description:Defining mechanism(s) that maintain tissue stem quiescence is important for improving tissue regeneration, cell therapies, aging, and cancer. We report here that genetic ablation of Id2 in adult hematopoietic stem cells (HSCs) promotes increased HSC activation and differentiation, which results in HSC exhaustion and bone marrow failure over time. Id2Δ/Δ HSCs show increased cycling, reactive oxygen species (ROS) production, mitochondrial activation, ATP production, and DNA damage compared to Id2+/+ HSCs, supporting the conclusion that Id2Δ/Δ HSCs are less quiescent. Mechanistically, HIF-1α expression is decreased in Id2Δ/Δ HSCs, and stabilization of HIF-1α in Id2Δ/Δ HSCs restores HSC quiescence and rescues HSC exhaustion. ID2 promotes HIF-1α expression by binding to the Von Hippel-Lindau (VHL) protein and interfering with proteasomal degradation of HIF-1α. HIF-1α promotes Id2 expression and enforces a positive feedback loop between ID2 and HIF-1α to maintain HSC quiescence. Thus, sustained ID2 expression could protect HSCs during stress, and improve HSC expansion for gene editing and cell therapies.

2022-05-31 | GSE205102 | GEO

IGR_VHL_GE

Project description:VHL is a tumor suppressor gene involved in the oxygen-sensing pathway whose germline mutations predispose to distinct phenotypes. Heterozygous mutations predispose to von Hippel-Lindau disease characterized by the development of multiple tumors (including hemangioblastomas, renal cell carcinomas and pheochromocytomas)1-3. More recently, a specific VHL-R200W mutation was shown to be responsible for Chuvash Polycythemia in homozygous carriers whereas heterozygous individuals have no clinical manifestation4. We report here a family carrying, on the same allele, VHL mutations characteristics of the two types of disease (a Chuvash polycythemia-R200W mutation and a von Hippel-Lindau disease-R161Q mutation). Genotyping, modeling analysis and functional studies, including transcriptomic profile of the distinct mutants validated for the first time on direct HIF target genes, show a gradual capacity of the VHL mutants to regulate the hypoxia responsive pathway that correlate with the severity of the developed phenotype. Our study provide original results that illuminate genotype/phenotype correlations in von Hippel-Lindau disease.

2013-09-03 | E-MTAB-1269 | biostudies-arrayexpress

RNA expression data from kidneys lacking von Hippel-Lindau (VHL) protein in tubular epithelial cells

Project description:The cellular response to low oxygen supply is mediated by hypoxia-inducible factors (HIF). Under hypoxic conditions, HIF is stabilized and target genes are induced. Under normoxia, however, HIF is ubiquitinated through the von Hippel-Lindau protein (VHL), which results in proteasomal degradation. HIF activation leads to induction of genes involved in erythropoiesis, angiogenesis, and cell survival. Furthermore, HIF orchestrates a metabolic shift from oxidative phosphorylation to glycolysis to facilitate ATP production under low oxygen conditions. We used microarrays to detail gene expression changes in kidneys with stable HIF activation in renal tubules, which was achieved by tubule-specific VHL ablation. Three week old Pax8-rtTA;LC-1;Vhl-floxed mice (n=4) and control littermates (n=4) were treated with doxycyline in drinking water for two weeks and put back on normal drinking water for one week. Six weeks old mice were sacrificed and kidneys harvested. Total RNA was extracted and hybridized on Affymetrix microarrays.

2014-01-17 | E-GEOD-54172 | biostudies-arrayexpress

Genetic Analysis of Pathways Regulated by the von Hippel-Lindau Tumor Suppressor in Caenorhabditis elegans

Project description:The von Hippel-Lindau (VHL) tumor suppressor functions as a ubiquitin ligase that mediates proteolytic inactivation of hydroxylated a subunits of hypoxia-inducible factor (HIF). Although studies of VHL defective renal carcinoma cells suggest the existence of other VHL tumor suppressor pathways, dysregulation of the HIF transcriptional cascade has extensive effects that make it difficult to distinguish whether, and to what extent, observed abnormalities in these cells represent effects on pathways that are distinct from HIF. Here, we report on a genetic analysis of HIF dependent and independent effects of VHL inactivation by studying gene expression patterns in C. elegans. We show tight conservation of the HIF-1/VHL-1/EGL-9 hydroxylase pathway. However, persisting differential gene expression in hif-1 versus hif-1; vhl-1 double mutant worms clearly distinguished HIF-1 independent effects of VHL-1 inactivation. Genomic clustering, predicted functional similarities, and a common pattern of dysregulation in both vhl-1 worms and a set of mutants (dpy-18, let-268, gon-1, mig-17 and unc-6), with different defects in extracellular matrix formation, suggest that dysregulation of these genes reflects a discrete HIF-1 independent function of VHL-1 that is connected with extracellular matrix function. Set of arrays organized by shared biological context, such as organism, tumors types, processes, etc. Bishop T, Lau KW, Epstein AC, Kim SK, Jiang M, O'rourke D, Pugh CW, Gleadle JM, Taylor MS, Hodgkin J, Ratcliffe PJ, Genetic Analysis of Pathways Regulated by the von Hippel-Lindau Tumor Suppressor in Caenorhabditis elegans., Bishop T, et al. (2004) PLoS Biol 2(10):e289, 2004-10-01, http://biology.plosjournals.org/plosonline/?request=get-document&doi=10.1371/journal.pbio.0020289 Computed

2005-07-20 | E-GEOD-2963 | biostudies-arrayexpress

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