Affymetrix arrays comparing 1) the transcriptome of Zeb1 or Hif1 expressing CGNs & 2) the transcriptome of hypoxia treated CGNs
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ABSTRACT:
ORGANISM(S): Mus musculus
SUBMITTER: David Solecki
PROVIDER: E-MTAB-8761 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
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Project description:This experiment captures the expression data obtained from mouse cerebellar granule neurons (CGN) at different time points of post-natal development, both in wild type samples (P0, P7, and P15) and in CGN electroporated with vectors expressing transcription factors Zeb1 and Hes1 (both P7).
2016-05-17 | E-MTAB-3557 | biostudies-arrayexpress
Project description:Dendrite and synapse development are critical for establishing appropriate neuronal circuits, and disrupted timing of these events can alter connectivity leading to disordered neural function. In early postnatal development of cerebellar granule neurons (CGNs), the expression of many genes is temporally regulated. Further, NFI (Nuclear Factor I) proteins have been shown to play important roles in the regulation of gene expression in developing CGNs. To identify NFI-regulated genome-wide targets involved in late maturation of mouse CGNs, we performed two groups of microarray expression analysis: (1) temporal expression arrays using 1.5 and 6 day cultures of mouse CGNs representing immature and more mature CGNs, respectively, which identified 844 Temporal-Up or Down genes; and (2) NFI-regulated genes in 6 day CGN cultures that were infected at the time of plating with lentiviral vectors expressing either NFI dominant repressor (NFI-EnR) or EnR control protein. This identified 686 NFI-Up (NFI-EnR down-regulated) or NFI-Down (NFI-EnR up-regulated) genes. Overlap analysis identified 212 temporal genes that were regulated by NFI. These results indicated that NFI plays a pivotal role in the regulation of late CGN maturation. For temporal arrays, mouse CGN progenitors were purified from P6 mouse cerebellum and cultured for either 1.5 or 6 days. Three biological replicates were analyzed for each time point. For NFI arrays, CGN progenitors from P6 mice were transduced upon plating with either NFI-EnR or EnR control lentivirus and cultured 6 days. Four pairs of biological replicates were performed.
2012-11-07 | E-GEOD-42018 | biostudies-arrayexpress
Project description:Expression analysis was performed with in vitro cultured cerebellar granule neurons (CGNs) isolated from rat brain. The CGNs were culture for four weeks. Each sample was collected after interval of seven days. No treatment was given to any cultured neurons at any time point. The purpose of the experiment was to identify the genes differentially expressed during the senescence of CGNs. The experiment is useful in revealing the senescence associated genetic markers in neurons.
2016-03-07 | E-MTAB-4552 | biostudies-arrayexpress
Project description:We report the high-throughput profilings of HIF1 and histone modifications in human umbilical vein endothelial cells (HUVEC). By obtaining over two billion bases of sequence from chromatin immunoprecipitated DNA, we generated genome-wide chromatin-state maps of HUVEC under normoxia and hypoxia. We find that HIF1binds to not only to transcriptional starting sites but also enhancer regions and that HIF1 binding sites were overlapped with lysine 4 trimethylatio, monomethylation and lysine 27 acetylation . Finally, we show that chromatin state can change under hypoxia by using chromatin conformational capture assay. This study provides novel insights into the interaction between HIF1 and KDM3A and also the epigenetic regulation of HIF1. Examination of HIF1 and 3 different histone modifications in HUVEC under 2 conditions. Related gene expression data is provided in GSE35932.
2012-07-12 | E-GEOD-39089 | biostudies-arrayexpress
Project description:Ischemic heart disease is a leading cause of heart failure and hypoxia inducible factor 1 (HIF1) has been shown to be a key transcription factor in the early response to hypoxic injury. We previously developed an inducble model of cardiomyopathy using cardiomyocyte-specific expression of a mutated, oxygen-stable form of HIF-1⍺ (HIF-PPN). In this study, we used high throughput sequencing to explore HIF1-mediated transcriptional changes in the heart.
2021-06-15 | GSE148351 | GEO
Project description:Although it has been shown that HIF1 and 2 fulfill essential roles within the hematopoietic system and in the regulation of HSC fate, little is currently known about the specific mechanisms that are involved. We identified transcriptome changes induced by hypoxia, constitutively active HIF1(P402/564) and HIF2(P405/531) in human cord blood CD34+ cells. Thus, we were able to identify common hypoxia-HIF1-HIF2 gene signatures, but we also identified specific target genes that were exclusively regulated by HIF1, HIF2 or hypoxia.
2014-03-01 | GSE54662 | GEO
Project description:Glioblastoma (GBM) is characterized by a high degree of hypoxia. Hypoxia-inducible factors (HIFs) modulate glioma stem-like cell (GSC) responses to hypoxia and promote GBM progression, therapeutic resistance, and recurrence. Here we identify a new transcript of the long non-coding RNA LUCAT1 and show that it reinforces HIF1⍺ signaling in GSCs under hypoxia. LUCAT1 expression is highly induced under hypoxia in GBM and GSCs in a HIF1⍺-dependent manner. High LUCAT1 expression in human GBM correlates with increased aggression and poor survival. Mechanistically, LUCAT1 associates with chromatin and modulates interaction between HIF1⍺ and coactivator CBP to hypoxia response elements (HREs) to drive HIF1⍺-target gene expression under hypoxia. Thus, LUCAT1 acts as a positive feedback factor to augment HIF1⍺ signaling under hypoxic stress in GSCs. Loss of LUCAT1 reduces tumor growth and prolongs mouse survival in xenograft models of GBM. Our findings provide new insights into how GSCs regulate gene expression under hypoxia and identify LUCAT1 as therapeutic target in GBM.
2024-03-12 | GSE255501 | GEO
Project description:Glioblastoma (GBM) is characterized by a high degree of hypoxia. Hypoxia-inducible factors (HIFs) modulate glioma stem-like cell (GSC) responses to hypoxia and promote GBM progression, therapeutic resistance, and recurrence. Here we identify a new transcript of the long non-coding RNA LUCAT1 and show that it reinforces HIF1⍺ signaling in GSCs under hypoxia. LUCAT1 expression is highly induced under hypoxia in GBM and GSCs in a HIF1⍺-dependent manner. High LUCAT1 expression in human GBM correlates with increased aggression and poor survival. Mechanistically, LUCAT1 associates with chromatin and modulates interaction between HIF1⍺ and coactivator CBP to hypoxia response elements (HREs) to drive HIF1⍺-target gene expression under hypoxia. Thus, LUCAT1 acts as a positive feedback factor to augment HIF1⍺ signaling under hypoxic stress in GSCs. Loss of LUCAT1 reduces tumor growth and prolongs mouse survival in xenograft models of GBM. Our findings provide new insights into how GSCs regulate gene expression under hypoxia and identify LUCAT1 as therapeutic target in GBM.
2024-03-12 | GSE255502 | GEO
Project description:HIF1 is essential for regulation of the transcriptional response to hypoxia. Recently we showed that the transcriptional repressors E2F7 and E2F8 interact and transcriptionally cooperate with HIF1. Here we further explored this cooperation by performing genome-wide analysis, screening for novel HIF1-E2F7 targets. We show that specifically E2F7 is induced in hypoxia by HIF1. Furthermore, chip-sequencing for E2F7 and HIF1 revealed a large number of common targets of which a subset was also regulated by the complex as examined by microarray analysis. Our data show that the HIF1-E2F7 complex can function both as a repressor or activator. Notably, we identify neuropilin 1 (NRP1) as a novel HIF1-E2F7 target, which is repressed by HIF1-E2F7 in vitro and during zebrafish development, depending on E2F-binding sites present in the NRP1 promoter. In addition we show that regulation of NRP1 by the HIF1-E2F7 complex is required for normal axon guidance of spinal motorneurons in vivo. ChIP-seq analysis of HIF1a and E2F7 binding
2015-12-11 | E-GEOD-66956 | biostudies-arrayexpress
Project description:To identify chromatin mechanisms of neuronal differentiation, we characterized the relationship between chromatin accessibility and gene expression in cerebellar granule neurons (CGNs) of the developing mouse. We used DNase-seq to globally map accessibility of cis-regulatory elements and RNA-seq to profile transcript abundance at key points in postnatal neuronal differentiation in vivo and in culture. We observed thousands of chromatin accessibility changes as CGNs differentiated and determined that many of these regions function as stage-specific neuronal enhancers. Motif discovery within differentially accessible chromatin regions suggested a novel role for the Zic family of transcription factors in CGN maturation, and we confirmed the association of Zic with these elements by ChIP-seq. Knockdown of Zic1 and Zic2 indicated Zic transcription factors are required to coordinate mature neuronal gene expression patterns. These data reveal chromatin dynamics at thousands of gene regulatory elements that facilitate gene expression patterns necessary for neuronal differentiation and function. Biological triplicate DNase-seq and RNA-seq samples from 3 in vivo cerebellum developmental stages (P7, P14, P60) and 3 cultured CGN stages (isolated granule neuron precursors, +3DIV, and +7DIV) obtained. Zic1 and Zic2 were separately knocked down by lentiviral shRNA in cultured CGNs followed by RNA-seq (2 biological replicates per KD and 2 controls). Zic1/2 ChIP-seq was performed with in vivo cerebellum at two developmental stages (P7 and P60) in duplicate with matching input and IgG controls.
2015-02-27 | E-GEOD-60731 | biostudies-arrayexpress