Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

GENERATION OF MOUSE NEOCORTICAL ORGANOIDS TO MODEL THE IMPACT OF CIS-REGULATORY VARIATION ON CORTICAL NEUROGENESIS ACROSS EVOLUTIONARY TIMESCALES

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus Mus

PROVIDER: GSE268333 | GEO | 2024/10/20

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

GENERATION OF MOUSE NEOCORTICAL ORGANOIDS TO MODEL THE IMPACT OF CIS-REGULATORY VARIATION ON CORTICAL NEUROGENESIS ACROSS EVOLUTIONARY TIMESCALES (scRNA-Seq)

Project description:Natural selection has shaped the gene regulatory networks that orchestrate the development of the neocortex, leading to diverse neocortical structure and function across mammals, but the molecular and cellular mechanisms driving phenotypic changes have proven difficult to characterize. Here, we develop a reproducible protocol to generate cortical organoids from mouse epiblast stem cells that enable in depth mechanistic studies of cortical developmental in vitro. Cortical organoids develop with similar kinetics to the mouse cortex in vivo, recapitulate the cellular diversity present in the embryonic neocortex, and undergo relatively rapid maturation compared to human organoids. We generated cortical organoids from F1 hybrid epiblast stem cell lines from crosses between standard laboratory mice (C57Bl/6J) and four wild-derived inbred mouse strains from distinct sub-species that span ~1 million years of evolutionary divergence. Using scRNA-seq and allele-specific expression analysis we identified hundreds of genes that exhibit differential cis-regulation during cortical neurogenesis. These experimental methods and cellular resources represent a powerful new platform for investigating gene regulatory mechanisms across evolutionary timescales.

2024-10-20 | GSE268332 | GEO

GENERATION OF MOUSE NEOCORTICAL ORGANOIDS TO MODEL THE IMPACT OF CIS-REGULATORY VARIATION ON CORTICAL NEUROGENESIS ACROSS EVOLUTIONARY TIMESCALES (scATAC-Seq)

2024-10-20 | GSE268331 | GEO

GENERATION OF MOUSE NEOCORTICAL ORGANOIDS TO MODEL THE IMPACT OF CIS-REGULATORY VARIATION ON CORTICAL NEUROGENESIS ACROSS EVOLUTIONARY TIMESCALES (bulk RNA-Seq)

2024-10-20 | GSE268329 | GEO

GENERATION OF MOUSE NEOCORTICAL ORGANOIDS TO MODEL THE IMPACT OF CIS-REGULATORY VARIATION ON CORTICAL NEUROGENESIS ACROSS EVOLUTIONARY TIMESCALES

Project description:GENERATION OF MOUSE NEOCORTICAL ORGANOIDS TO MODEL THE IMPACT OF CIS-REGULATORY VARIATION ON CORTICAL NEUROGENESIS ACROSS EVOLUTIONARY TIMESCALES

| PRJNA1116220 | ENA

GENERATION OF MOUSE NEOCORTICAL ORGANOIDS TO MODEL THE IMPACT OF CIS-REGULATORY VARIATION ON CORTICAL NEUROGENESIS ACROSS EVOLUTIONARY TIMESCALES (scATAC-Seq)

Project description:GENERATION OF MOUSE NEOCORTICAL ORGANOIDS TO MODEL THE IMPACT OF CIS-REGULATORY VARIATION ON CORTICAL NEUROGENESIS ACROSS EVOLUTIONARY TIMESCALES (scATAC-Seq)

| PRJNA1116225 | ENA

GENERATION OF MOUSE NEOCORTICAL ORGANOIDS TO MODEL THE IMPACT OF CIS-REGULATORY VARIATION ON CORTICAL NEUROGENESIS ACROSS EVOLUTIONARY TIMESCALES (scRNA-Seq)

Project description:GENERATION OF MOUSE NEOCORTICAL ORGANOIDS TO MODEL THE IMPACT OF CIS-REGULATORY VARIATION ON CORTICAL NEUROGENESIS ACROSS EVOLUTIONARY TIMESCALES (scRNA-Seq)

| PRJNA1116224 | ENA

GENERATION OF MOUSE NEOCORTICAL ORGANOIDS TO MODEL THE IMPACT OF CIS-REGULATORY VARIATION ON CORTICAL NEUROGENESIS ACROSS EVOLUTIONARY TIMESCALES (bulk RNA-Seq)

Project description:GENERATION OF MOUSE NEOCORTICAL ORGANOIDS TO MODEL THE IMPACT OF CIS-REGULATORY VARIATION ON CORTICAL NEUROGENESIS ACROSS EVOLUTIONARY TIMESCALES (bulk RNA-Seq)

| PRJNA1116227 | ENA

Human SPG11 cerebral organoids reveal cortical neurogenesis impairment.

Project description:Spastic paraplegia gene 11(SPG11)-linked hereditary spastic paraplegia is a complex monogenic neurodegenerative disease that in addition to spastic paraplegia is characterized by childhood onset cognitive impairment, thin corpus callosum and enlarged ventricles. We have previously shown impaired proliferation of SPG11 neural progenitor cells (NPCs). For the delineation of potential defect in SPG11 brain development we employ 2D culture systems and 3D human brain organoids derived from SPG11 patients' iPSC and controls. We reveal that an increased rate of asymmetric divisions of NPCs leads to proliferation defect, causing premature neurogenesis. Correspondingly, SPG11 organoids appeared smaller than controls and had larger ventricles as well as thinner germinal wall. Premature neurogenesis and organoid size were rescued by GSK3 inhibititors including the Food and Drug Administration-approved tideglusib. These findings shed light on the neurodevelopmental mechanisms underlying disease pathology.

| S-EPMC6400051 | biostudies-literature

Chromatin features constrain structural variation across evolutionary timescales.

Project description:The potential impact of structural variants includes not only the duplication or deletion of coding sequences, but also the perturbation of noncoding DNA regulatory elements and structural chromatin features, including topological domains (TADs). Structural variants disrupting TAD boundaries have been implicated both in cancer and developmental disease; this likely occurs via "enhancer hijacking," whereby removal of the TAD boundary exposes enhancers to new target transcription start sites (TSSs). With this functional role, we hypothesized that boundaries would display evidence for negative selection. Here we demonstrate that the chromatin landscape constrains structural variation both within healthy humans and across primate evolution. In contrast, in patients with developmental delay, variants occur remarkably uniformly across genomic features, suggesting a potentially broad role for enhancer hijacking in human disease.

| S-EPMC6369792 | biostudies-literature

Human Cortical Organoids Expose a Differential Function of GSK3 on Cortical Neurogenesis.

Project description:The regulation of the proliferation and polarity of neural progenitors is crucial for the development of the brain cortex. Animal studies have implicated glycogen synthase kinase 3 (GSK3) as a pivotal regulator of both proliferation and polarity, yet the functional relevance of its signaling for the unique features of human corticogenesis remains to be elucidated. We harnessed human cortical brain organoids to probe the longitudinal impact of GSK3 inhibition through multiple developmental stages. Chronic GSK3 inhibition increased the proliferation of neural progenitors and caused massive derangement of cortical tissue architecture. Single-cell transcriptome profiling revealed a direct impact on early neurogenesis and uncovered a selective role of GSK3 in the regulation of glutamatergic lineages and outer radial glia output. Our dissection of the GSK3-dependent transcriptional network in human corticogenesis underscores the robustness of the programs determining neuronal identity independent of tissue architecture.

| S-EPMC6893153 | biostudies-literature

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data