We found that PI3K inhibition increased the expression of stem cell markers in trophoblast stem cells (TSCs). To better understand the PI3K inhibited cells, we compared untreated TSCs with cells treated with PI3K inhibitor ZSTK474 for 3h, 6h and 3 days. Overall design: Untreated TSCs, TSCs treated with 200nM ZSTK474 for 3h, 6h, and 3 days.
Inhibition of Phosphoinositide-3-Kinase Signaling Promotes the Stem Cell State of Trophoblast.
Specimen part, Cell line, Subject, Time
View SamplesCritical roles for DNA methylation in embryonic development are well established, but less is known about the roles of DNA methylation during trophoblast development, the extraembryonic lineage that gives rise to the placenta. Here we dissected the role of DNA methylation in trophoblast development by performing mRNA and DNA methylation profiling of Dnmt3a/3b-null trophoblast. We find that most gene deregulation is explained by an erasure of maternal methylation in the oocyte, but partially independent of loss of imprinting of the trophoblast-essential Ascl2 gene. Our results reveal that maternal DNA methylation controls multiple differentiation and physiological processes in trophoblast via both imprinting-dependent and -independent mechanisms. Overall design: mRNA-seq and WGBS-seq of maternal Dnmt3a/3b-null trophoblast; mRNA-seq of maternal Ascl2 KO trophoblast
Maternal DNA Methylation Regulates Early Trophoblast Development.
No sample metadata fields
View SamplesExpression profiling in hippocampal neurons to identify activity-regulated genes controlled by MEF2
Genome-wide analysis of MEF2 transcriptional program reveals synaptic target genes and neuronal activity-dependent polyadenylation site selection.
No sample metadata fields
View SamplesExpression profiling in hippocampal neurons to identify genes upregulated in response to ectopic MEF2 activation by MEF2-VP16-ER
Genome-wide analysis of MEF2 transcriptional program reveals synaptic target genes and neuronal activity-dependent polyadenylation site selection.
No sample metadata fields
View SamplesExpression profiling in whole rat forebrain in response to exposure of animals to a novel environment
Genome-wide analysis of MEF2 transcriptional program reveals synaptic target genes and neuronal activity-dependent polyadenylation site selection.
No sample metadata fields
View SamplesDisruption of the MECP2 gene leads to Rett syndrome (RTT), a severe neurological disorder with features of autism. MECP2 encodes a methyl-DNA-binding protein that is proposed to function as a transcriptional repressor, but, despite numerous studies examining neuronal gene expression in MeCP2 mutants, no coherent model has emerged for how MeCP2 regulates transcription. Here we identify a genome-wide length-dependent increase in the expression of long genes in neurons lacking MeCP2. This gene misregulation occurs in human RTT brains and correlates with onset and severity of phenotypes in Mecp2 mutant mice, suggesting that the disruption of long gene expression contributes to RTT pathology. We present evidence that MeCP2 represses long genes by binding to brain-enriched, methylated CA dinucleotides within genes and show that loss of methylated CA in the brain recapitulates gene expression defects observed in MeCP2 mutants. We find that long genes encode proteins with neuronal functions, and overlap substantially with genes that have been implicated in autism and Fragile X syndrome. Reversing the overexpression of long genes in neurons lacking MeCP2 can improve some RTT-associated cellular deficits. These findings suggest that a function of MeCP2 in the mammalian brain is to temper the expression of genes in a length-dependent manner, and that mutations in MeCP2 and possibly other autism genes may cause neurological dysfunction by disrupting the expression of long genes in the brain. Overall design: Total RNA-seq Data from the visual cortex of wild-type and MeCP2 knockout animals at 8-10 weeks of age
Disruption of DNA-methylation-dependent long gene repression in Rett syndrome.
No sample metadata fields
View SamplesWe report a new unsupervised clustering tool for single cell RNA-seq data called SC3. We show that biologically relevant information can be obtained from preneoplastic cells of patients with myeloprolifertive disease. Overall design: examination of three different patients with myeloproloferative disease
SC3: consensus clustering of single-cell RNA-seq data.
No sample metadata fields
View SamplesAlthough the induction of C-FOS in the brain has been extensively studied for several decades to date there has been no attempt to identify the targets of C-FOS at a genome wide level, and it was not known how many genes C-FOS activates in a given cell. To identify potential C-FOS target genes, we performed microarray analysis on RNA obtained from mouse cortical (mCTX) neurons infected with lentivirus containing either a control shRNA (targeting firefly luciferase) or c-Fos shRNA that were subsequently depolarized with 0, 1, 3, or 6 hours of KCl.
Genome-wide identification and characterization of functional neuronal activity-dependent enhancers.
Specimen part
View SamplesJAK2 activation by TPO study and its downstream targets STAT1, STAT3 and STAT5 on Mouse HPC7 stem cells on four time points. The aim is to verify wether a JAK/STAT signalling signature is similar to the age-related functional decline in the haematopoietic system.
Proliferation Drives Aging-Related Functional Decline in a Subpopulation of the Hematopoietic Stem Cell Compartment.
Cell line, Treatment, Time
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Single-cell transcriptomics reveals a new dynamical function of transcription factors during embryonic hematopoiesis.
Specimen part, Disease, Cell line, Treatment
View Samples