Global expression analysis of neural crest-like skin-derived precursors (SKPs) and Sox2-positive follicle dermal cells that SKPs originate from.
SKPs derive from hair follicle precursors and exhibit properties of adult dermal stem cells.
Specimen part
View SamplesThe overall goal of our studies is to elucidate the cellular and molecular mechanism by which the transcription factor Casz1 functions in murine heart development. We established that Casz1 is expressed in myocardial progenitor cells beginning at E7.5 and in differentiated cardiomyocytes throughout development. We generated conditional Casz1 knockout mice to show that ablation of CASZ1 in Nkx2.5-positive cardiomyocytes leads to cardiac hypoplasia, ventricular septal defects and lethality by E13.5. To identify the pathways and networks by which Casz1 regulates cardiomyocyte development, we used RNA-Seq and identified genes involved in cell proliferation are upregulated in Casz1 mutants compared to wild-type littermates. We conclude that Casz1 is essential for cardiac development and has a pivotal role in regulating part of the cardiac transcriptional program. Overall design: 3 biological replicates of the two genotypes (Nkx2-5+/+,Casz1f/+ and Nkx2-5Cre/+,Casz1f/f) were used for RNA-seq to determine genes that are differentially expressed in the murine heart when Casz1 is mutated. Nkx2-5+/+,Casz1f/+ were used as wild-type controls for comparison.
Casz1 is required for cardiomyocyte G1-to-S phase progression during mammalian cardiac development.
No sample metadata fields
View SamplesUsing Tbx18Cre to target embryonic DP precursors, we ablate Sox2 early and efficiently, resulting in diminished hair shaft outgrowth. Transcriptional profiling of Sox2 null DPs reveals increased Bmp6 and decreased Bmp inhibitor Sostdc1, a direct Sox2 transcriptional target.
Sox2 in the dermal papilla niche controls hair growth by fine-tuning BMP signaling in differentiating hair shaft progenitors.
Specimen part
View SamplesCardiac disease accounts for the largest proportion of adult mortality and morbidity in the industrialized world. However, progress toward improved clinical treatments is hampered by an incomplete understanding of the genetic programs controlling early cardiogenesis. To better understand this process, we set out to identify genes whose expression is enriched within early cardiac fated populations, obtaining the transcriptional signatures of mouse embryonic stem cells (mESCs) differentiating along a cardiac path.
Efficient array-based identification of novel cardiac genes through differentiation of mouse ESCs.
No sample metadata fields
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Cell isolation induces fate changes of bone marrow mesenchymal cells leading to loss or alternatively to acquisition of new differentiation potentials.
Specimen part
View SamplesMesenchymal populations include a fraction of cells exhibiting multipotency as well as others with limited differentiation range. It has been assumed that the mesenchymal cellular cascade is topped by a multipotent cell, which gives rise to progeny with diminishing differentiation potentials. Here we show that cultured mesenchymal cells, a priori exhibiting a limited differentiation potential, may gain new capacities and become multipotent following single cell isolation. These fate changes were accompanied by up-regulation of differentiation promoting genes, many of which also became H4K20me1 methylated. Early events in the process included TGF and Wnt modulation, and down-regulation of hypoxia signaling. Indeed, hypoxic conditions inhibited the observed cell changes. Overall, cell isolation from neighboring partners caused major molecular changes and particularly, a newly established epigenetic state. It is suggested that MSCs behave non-deterministically and non-hierarchically and should therefore be defined primarily by their capacity to undergo fate changes triggered by environmental cues.
Cell isolation induces fate changes of bone marrow mesenchymal cells leading to loss or alternatively to acquisition of new differentiation potentials.
Specimen part
View SamplesMesenchymal populations include a fraction of cells exhibiting multipotency as well as others with limited differentiation range. It has been assumed that the mesenchymal cellular cascade is topped by a multipotent cell, which gives rise to progeny with diminishing differentiation potentials. Here we show that cultured mesenchymal cells, a priori exhibiting a limited differentiation potential, may gain new capacities and become multipotent following single cell isolation. These fate changes were accompanied by up-regulation of differentiation promoting genes, many of which also became H4K20me1 methylated. Early events in the process included TGF and Wnt modulation, and down-regulation of hypoxia signaling. Indeed, hypoxic conditions inhibited the observed cell changes. Overall, cell isolation from neighboring partners caused major molecular changes and particularly, a newly established epigenetic state. It is suggested that MSCs behave non-deterministically and non-hierarchically and should therefore be defined primarily by their capacity to undergo fate changes triggered by environmental cues.
Cell isolation induces fate changes of bone marrow mesenchymal cells leading to loss or alternatively to acquisition of new differentiation potentials.
Specimen part
View SamplesRett syndrome (RTT, OMIM #312750) is a severe X-linked neurodevelopmental disorder linked to heterozygous de novo mutations in the MECP2 gene. MECP2 encodes methyl-CpG-binding protein 2 (MeCP2), which represses gene transcription by binding to 5-methylcytosine residues in symmetrically positioned CpG dinucleotides. The disorder is almost exclusively diagnosed in females, because males affected by the disease usually die perinatally due to severe encephalopathy. Direct MeCP2 target genes underlying the neuropathogenesis of RTT remain largely unknown.
FXYD1 is an MeCP2 target gene overexpressed in the brains of Rett syndrome patients and Mecp2-null mice.
No sample metadata fields
View SamplesCognitive deficit is a key feature of schizophrenia (SZ) and determines functional outcome. Nonetheless, molecular signatures underlying the deficit in neuronal tissues are not well understood.
Molecular signatures associated with cognitive deficits in schizophrenia: a study of biopsied olfactory neural epithelium.
Sex, Age, Specimen part, Race
View SamplesQuetiapine is an atypical neuroleptic with a pharmacological profile distinct from classic neuroleptics. It is currently approved for treating patients with schizophrenia, major depression and bipolar I disorder. However, its cellular effects remain elusive.
Unique pharmacological actions of atypical neuroleptic quetiapine: possible role in cell cycle/fate control.
Sex, Treatment
View Samples