Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Tissue-wide Genetic and Cellular Landscape Instructs the Execution of Sequential PRC2 Functions in Neural Stem Cell Lineage Progression [neurons]

ABSTRACT: Tissue-wide Genetic and Cellular Landscape Instructs the Execution of Sequential PRC2 Functions in Neural Stem Cell Lineage Progression [neurons]

PROVIDER: PRJNA789779 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR17256800.fastq.gz	Fastqsanger.gz
	SRR17256900.fastq.gz	Fastqsanger.gz
	SRR17257000.fastq.gz	Fastqsanger.gz
	SRR17256801.fastq.gz	Fastqsanger.gz
	SRR17256901.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 282

Similar Datasets

Tissue-wide Genetic and Cellular Landscape Instructs the Execution of Sequential PRC2 Functions in Neural Stem Cell Lineage Progression [neurons]

Project description:The generation of a correctly-sized cerebral cortex with all-embracing neuronal and glial cell-type diversity critically depends on faithful radial glial progenitor (RGP) cell proliferation/differentiation programs. Temporal RGP lineage progression is regulated by Polycomb Repressive Complex 2 (PRC2) and loss of PRC2 activity results in severe neurogenesis defects and microcephaly. How PRC2-dependent gene expression instructs RGP lineage progression is unknown. Here we utilize Mosaic Analysis with Double Markers (MADM)-based single cell technology and demonstrate that PRC2 is not cell-autonomously required in neurogenic RGPs but rather acts at the global tissue-wide level. Conversely, cortical astrocyte production and maturation is cell-autonomously controlled by PRC2-dependent transcriptional regulation. We thus reveal highly distinct and sequential PRC2 functions in RGP lineage progression that are dependent on complex interplays between intrinsic and tissue-wide mechanisms. In a broader context our results imply a critical role for the genetic and cellular niche environment in neural stem cell behavior.

2022-09-12 | GSE191108 | GEO

Tissue-wide Genetic and Cellular Landscape Instructs the Execution of Sequential PRC2 Functions in Neural Stem Cell Lineage Progression [astro]

2022-09-12 | GSE191107 | GEO

Tissue-wide Genetic and Cellular Landscape Instructs the Execution of Sequential PRC2 Functions in Neural Stem Cell Lineage Progression

Project description:Tissue-wide Genetic and Cellular Landscape Instructs the Execution of Sequential PRC2 Functions in Neural Stem Cell Lineage Progression

| PRJNA789777 | ENA

Tissue-wide Genetic and Cellular Landscape Instructs the Execution of Sequential PRC2 Functions in Neural Stem Cell Lineage Progression [astro]

Project description:Tissue-wide Genetic and Cellular Landscape Instructs the Execution of Sequential PRC2 Functions in Neural Stem Cell Lineage Progression [astro]

| PRJNA789773 | ENA

Tissue-wide Genetic and Cellular Landscape Instructs the Execution of Sequential PRC2 Functions in Neural Stem Cell Lineage Progression

Project description:This SuperSeries is composed of the SubSeries listed below.

2022-09-12 | GSE191109 | GEO

Tissue-wide genetic and cellular landscape shapes the execution of sequential PRC2 functions in neural stem cell lineage progression.

Project description: Not available

| S-EPMC9629739 | biostudies-literature

PRC2

Project description:PRC2

| PRJNA761389 | ENA

Functional Comparison to Ezh2 Reveals PRC2-Independent Functions of Jarid2 in Hematopoietic Stem Cell Lineage Commitment

Project description:Our previous studies showed the Polycomb Repressive Complex 2 (PRC2) co-factor Jarid2 represses self-renewal transcriptional networks in mouse multipotent progenitor cells (MPPs). But only a fraction of de-repressed HSC-specific genes were associated with loss of H3K27me3, implying Jarid2 may have non-canonical (PRC2-indpendent) in hematopoiesis. Here we sought to delineate any PRC2-independnent functions by comparing stem and progenitor cells genetically deficient for either Jarid2 or Ezh2. Loss of Ezh2 leads to increased myeloid differentiation in transplantation assays. In contrast, loss of Jarid2 enhanced T-cell output. Single cell transcriptomics showed while loss of Jarid2 had minimal impact across progenitor populations, loss of Ezh2 led to accumulation of lymphoid-biased MPP4 cells and B-cell progenitors in the bone marrow. Functional assays confirmed a differentiation block at the pre-pro B-cell stage. The maturational arrest of Ezh2-deficient B-cell progenitors contrasts with increased T-cell output from loss of Jarid2, suggesting Jarid2 has non-canonical functions in hematopoiesis.

2025-11-17 | GSE302605 | GEO

Auto-inhibition of PRC2 by the broadly expressed long isoform of AEBP2.

Project description:Polycomb Repressive Complex 2 (PRC2) is an essential chromatin regulator responsible for mono-, di- and tri- methylating H3K27. Control of PRC2 activity is a critical process in development and disease. While PRC2 is inhibited in germinal cells, no inhibitory cofactor has been identified in somatic cells. Here we show that the alternative isoforms of its accessory subunit AEBP2, namely AEPB2S (short) and AEBP2L (long), perform opposite functions in modulating PRC2 activity. While AEPB2S is predominantly expressed during early embryogenesis, AEBP2L is expressed throughout embryogenesis and adulthood. AEPB2L inhibits both DNA binding by PRC2 and its histone methyltransferase activity in vitro and impairs PRC2 binding to target genes in embryonic stem cells. In contrast, AEBP2S promotes the DNA-binding activity of PRC2 and is essential for de novo repression of target genes during the transition from naïve to primed pluripotency. Mechanistically, through high-resolution Cryo-EM and mutagenesis, we show that the recently evolved, negatively charged N-terminal region of AEBP2L inhibits PRC2. We propose a model in which the N-terminus of AEPB2L arose in vertebrates to restrain PRC2 in somatic cells.

2025-08-26 | PXD053693 | Pride

A TET1-PSPC1-Neat1 molecular axis modulates PRC2 functions in controlling stem cell bivalency [RNA-seq]

Project description:The mammalian Ten-eleven translocation (TET) family proteins regulate the epigenome through catalytic activity (CA)-dependent and -independent functions. While catalytic activity of TETs has been intensely studied as DNA demethylation enzymes, little is known about their CA-independent function in early embryo development. Here we defined the CA-independent function of TET1 in naïve-to-formative pluripotent states transition. Using a proteomics method, we mapped the TET1 interactome and identified Paraspeckle component 1 (PSPC1) as a partner of TET1 for transcriptional repression at the bivalent genes in early development. Genome-wide location analysis revealed that PSPC1-bound regions largely overlap with TET1 and Polycomb repressive complex 2 (PRC2) subunits. Functional studies with genetic methods indicated that PSPC1 and TET1 repress, while lncRNA Neat1 activates the bivalent genes during their transcriptional activation. In embryonic stem cell (ESC) state, Neat1 tethers TET1, PSPC1, and PRC2 at promoters. During the ESCs to formative Epiblast like stem cells (EpiLCs) differentiation, PSPC1 and TET1 repress the PRC2 affinity to nascent mRNA transcripts of bivalent genes, while Neat1 facilitates PRC2 binding to those transcripts. Our study reveals a molecular mechanism by which proteins TET1 and PSPC1, and lncRNA Neat1 dynamically regulate gene transcription by modulating the PRC2 activity in pluripotent states transition.

2022-06-07 | GSE182441 | GEO

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