Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA276909 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR1822610.fastq.gz | Fastqsanger.gz | |||
| SRR1822611.fastq.gz | Fastqsanger.gz | |||
| SRR1822612.fastq.gz | Fastqsanger.gz | |||
| SRR1822613.fastq.gz | Fastqsanger.gz | |||
| SRR1822614.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 11 |
Similar Datasets
Project description:Cortical development is a tightly spatiotemporally regulated process in which cell-fate specification is accompanied by stable resetting of transcriptional programs. However, the full repertoire of transcriptional regulators orchestrating such transcriptome changes remains largely incomprehensive. Applying a bioinformatics predictive approach we aimed to identify novel transcription factors contriuting to transcriptional reprogramming during embryonic neurogenesis and identified the neuronal tissue specific transcription factor St18 to be essential for neurogenesis in vitro and in vivo. We find that embryonic stem cells deficient for St18 are not able to efficiently differentiate along neuronal lineage and St18 depleted cells in the developing cortex do not elongate in shape and reside in the VZ/SVZ region but display premature expression of the upper layer neuronal marker Satb2. Relation of St18 binding to genes deregulated upon St18 depletion in vivo revealed St18 to function as transcriptional repressor at the time when neurogenesis is initiated. St18 ensures efficient onset of cortical neurogenesis by inhibiting expression of the self-renewal maintaining factor Hes1 that represses differentiation genes in neuronal progenitors as well as downregulation of genes that are essential for differentiation into mesodermal and endodermal lineage such as Lama5, Traf4 and Tab1. Furthermore we find this transcriptional repressor to be bound to genes that are important for later stages of neurogenesis when the neuronal circuitry is established likely to keep them in repressed state in the time window of neurogenesis when they are not yet required. These genes important for axon guidance and neurite outgrowth are subsequently prematurely upregulated in St18 depleted cortical cells. We further observe St18 to be bound to a significant fraction of intergenic enhancers where it regulates expression of nearest genes that Our data establish St18 as a novel transcriptional regulator during early onset of cortical neurogenesis that is essential to ensure timely expression kinetics of phase and lineage specific genes.
2021-02-01 | GSE66436 | GEO
Project description:Proper cortical development relies on the balance of neuronal migration and proliferation. We investigated the gene expression differences of mouse knock-outs for Lissencephaly in humans. Our analysis suggests that gene expression and pathway analysis in mouse models of a similar disorder or within a common pathway can be used to define novel candidates for related human diseases.
2012-01-26 | GSE35366 | GEO
Project description:We recently identified heterozygous deletions of the gene TSHZ3, which encodes a Zn-finger transcription factor, in patients with a syndrome including autistic features and provided evidence in mice for a link between Tshz3 haploinsufficiency, defects in cortical projection neurons (CPNs) and autism spectrum disorder (ASD)-like abnormalities. To get more insight into when and where TSHZ3 is required for the proper development of the brain, we generated and characterized a novel mouse model of conditional Tshz3 deletion in projection neurons from postnatal day 2-3 onward. These mice exhibit altered cortical expression of genes encoding for synaptic components, electrophysiological and synaptic changes in layer 5 CPNs, impaired corticostriatal glutamate transmission and plasticity, as well as strong ASD-relevant behavioral deficits. These data, by revealing a crucial postnatal role of TSHZ3 in the development and function of the corticostriatal circuitry that might be determinant for ASD pathogenesis, offer a novel ASD model and further open the possibility for an early postnatal therapeutic window for the syndrome linked to TSHZ3 haploinsufficiency.
2021-09-10 | GSE119791 | GEO
Project description:Notochordal cells are considered as a rare cell type ensuring signaling function required for proper development and homeostasis in various tissues. We used single cell RNA sequencing (scRNA-seq) to characterize gene signature of notochordal-like cells and understand heterogeneity of co-emerging cell types during in vitro differentiation.
2023-11-11 | GSE237538 | GEO
Project description:<p>Developmental brain malformations are at the core of significant neurological diseases affecting many families in the United States and around the world. It is known that epilepsy, specific learning deficits and intellectual disability, cerebral palsy, and abnormalities of brain volume can be attributed in many cases to pathological malformations of the cerebral cortex. Although these consequences, such as epilepsy and intellectual disability, might appear broadly in the population as due to complex traits, this study's focus on those associated with cortical malformations highlights individual developmental pathways likely represented by innumerable and rare Mendelian alleles. Research has thus far uncovered dozens of genes responsible for these conditions and dissected the mechanisms underlying early cortical development in animals. However, this progress represents only the dawn of understanding the complex genetic network and neuronal architecture of the uniquely human cerebral cortex.</p> <p>The overall goal of this study is to define the genetic bases of human cerebral cortical development. This is accomplished through (1) the ascertainment of families with disorders of human brain development and malformation, (2) categorizing these using medical, physical and neuroimaging data, and (3) mapping and identifying the gene causing the disorder of cortical development, which can then be investigated for its normal expression and function, and role in human disease. </p>
| phs000492 | dbGaP
Project description:Genome-wide chromosome conformation during early human cortical development
| PRJNA339020 | ENA
Project description:We report the transcriptome profiling (RNAseq) in hepatoblast-derived tumors, without (untreated) or with ST18 knockdown (4h Doxy) (three independent samples for each condition). We find that ST18 knockdown in hepatoblast-derived tumors affects inflammation-associated genes.
2017-12-22 | GSE72403 | GEO
Project description:Proper cortical development relies on the balance of neuronal migration and proliferation. We investigated the gene expression differences of mouse knock-outs for Lissencephaly in humans. Our analysis suggests that gene expression and pathway analysis in mouse models of a similar disorder or within a common pathway can be used to define novel candidates for related human diseases. We investigated the developing brain of four mutants and wild-type mice using expression microarrays, bioinformatic analyses, and in vivo/in vitro experiments to address whether mutations in different members of the LIS1 neuronal migration complex lead to similar and/or distinct global gene expression alterations.
2012-01-26 | E-GEOD-35366 | biostudies-arrayexpress
Project description:We recently identified heterozygous deletions of the gene TSHZ3, which encodes a Zn-finger transcription factor, in patients with a syndrome including autistic features and provided evidence in mice for a link between Tshz3 haploinsufficiency, defects in cortical projection neurons (CPNs) and autism spectrum disorder (ASD)-like abnormalities. To get more insight into when and where TSHZ3 is required for the proper development of the brain, we generated and characterized a novel mouse model of conditional Tshz3 deletion in projection neurons from postnatal day 2-3 onward. These mice exhibit altered striatal expression of genes encoding for synaptic components, electrophysiological and synaptic changes in striatal cholinergic interneurons, , as well as ASD-relevant behavioral deficits. These data, by revealing a crucial postnatal role of TSHZ3 in the development and function of the corticostriatal circuitry that might be determinant for ASD pathogenesis, offer a novel ASD model and further open the possibility for an early postnatal therapeutic window for the syndrome linked to TSHZ3 haploinsufficiency.
2020-09-09 | GSE157658 | GEO