Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Dlx1/2-Dependent Expression of Meis2 Promotes Neuronal Fate

ABSTRACT: Dlx1/2-Dependent Expression of Meis2 Promotes Neuronal Fate

PROVIDER: PRJNA779538 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR16915035_1.fastq.gz	Fastqsanger.gz
	SRR16915035_2.fastq.gz	Fastqsanger.gz
	SRR16915036_1.fastq.gz	Fastqsanger.gz
	SRR16915036_2.fastq.gz	Fastqsanger.gz

Items per page:

1 - 4 of 4

Similar Datasets

Dlx1/2-Dependent Expression of Meis2 Promotes Neuronal Fate Determination in the Mammalian Striatum

Project description:Dlx1/2-Dependent Expression of Meis2 Promotes Neuronal Fate Determination in the Mammalian Striatum

| PRJNA755886 | ENA

Dlx1/2-Dependent Expression of Meis2 Promotes Neuronal Fate Determination in the Mammalian Striatum [RNA-seq]

Project description:Dlx1/2-Dependent Expression of Meis2 Promotes Neuronal Fate Determination in the Mammalian Striatum [RNA-seq]

| PRJNA755894 | ENA

Stability of the neuronal fate determinant MEIS2 is controlled by calpain2

Project description:Calpains are non-lysosomal, Ca2+-dependent cysteine proteases, which are associated with various cellular functions but have so far been mainly studied in the context of disease. Their contribution to homeostasis in the healthy organism is still not well understood and their substrates have remained enigmatic in most cases. In the present study, we describe a previously unrecognized role for the calpain protease calpain2 in the regulation of neuronal differentiation of adult neural stem- and progenitor cells through cleavage and elimintation of the neuronal fate determinant MEIS2. Mass spectrometry analysis was performed on immunoprecipitated MEIS2 protein to identify phosphory¬lated residues in MEIS2 and on immunoprecipitated MEIS2 incubated with native porcine calpain2 to map calpain2-induced cleavage sites in the protein.

2024-02-08 | PXD036442 | Pride

Dlx1/2-Dependent Expression of Meis2 Promotes Neuronal Fate Determination in the Mammalian Striatum [CUT-Tag-seq]

Project description:Dlx1/2-Dependent Expression of Meis2 Promotes Neuronal Fate Determination in the Mammalian Striatum [CUT-Tag-seq]

| PRJNA751035 | ENA

Dlx1/2-Dependent Expression of Meis2 Promotes Neuronal Fate Determination in the Mammalian Striatum [CUT-Tag-seq]

Project description:Purpose:To identity genomic loci where MEIS2 binds at E14.5 in the LGE Methords: The CUT&Tag assay was performed using E14.5 LGEs dissected from wild-type CD1 mice and a MEIS2 mouse polyclonal antibody as described previously. Results: We derived a set of 13992 loci based on the presence of significant enrichment in MEIS2 libraries and no enrichment in the negative control datasets

2021-08-06 | GSE181192 | GEO

Dlx1/2-Dependent Expression of Meis2 Promotes Neuronal Fate Determination in the Mammalian Striatum [RNA-seq]

Project description:Purpose:To asses changes in gene expression profiles from the E14.5 littermate controls LGE and Meis2-CKO mice. Methods:The LGEs from E14.5 Meis2-CKO mutant and Control brains (n = 4 per group) were dissected, and RNA was isolated with the Direct-zol RNA Miniprep kit (Zymo, catalog #R2050) following the manufacturer’s instructions. Results: Identified 161 genes with downregulated RNA expression and 94 genes with upregulated RNA expression

2021-08-19 | GSE182335 | GEO

Dlx1/2-dependent expression of Meis2 promotes neuronal fate determination in the mammalian striatum.

Project description:The striatum is a central regulator of behavior and motor function through the actions of D1 and D2 medium-sized spiny neurons (MSNs), which arise from a common lateral ganglionic eminence (LGE) progenitor. The molecular mechanisms of cell fate specification of these two neuronal subtypes are incompletely understood. Here, we found that deletion of murine Meis2, which is highly expressed in the LGE and derivatives, led to a large reduction in striatal MSNs due to a block in their differentiation. Meis2 directly binds to the Zfp503 and Six3 promoters and is required for their expression and specification of D1 and D2 MSNs, respectively. Finally, Meis2 expression is regulated by Dlx1/2 at least partially through the enhancer hs599 in the LGE subventricular zone. Overall, our findings define a pathway in the LGE whereby Dlx1/2 drives expression of Meis2, which subsequently promotes the fate determination of striatal D1 and D2 MSNs via Zfp503 and Six3.

| S-EPMC8918808 | biostudies-literature

Dlx1/2-Dependent Expression of Meis2 Promotes Neuronal Fate

Project description:To acess chromatin accessibility of individual cell from striatum of E14.5 wild type mice.

2021-11-13 | GSE188602 | GEO

Dlx1/2-Dependent Expression of Meis2 Promotes Neuronal Fate Determination in the Mammalian Striatum

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

2021-08-19 | GSE182336 | GEO

DLX1 and the NuRD complex cooperate in enhancer decommissioning and transcriptional repression

Project description:In the developing subpallium, the fate decision between neurons and glia is driven by expression of Dlx1/2 or Olig1/2 respectively, two sets of transcription factors (TFs) with a mutually repressive relationship. The mechanism by which Dlx1/2 repress progenitor and oligodendrocyte fate, while promoting transcription of genes needed for differentiation, is not fully understood. We identified a motif within DLX1 that binds RBBP4, a NuRD complex subunit. ChIP-seq studies of genomic occupancy of DLX1 and six different members of the NuRD complex show that DLX1 and NuRD colocalize to putative regulatory elements (pREs) enriched near other transcription factor genes. Loss of Dlx1/2 leads to dysregulation of genome accessibility at pREs near genes repressed by Dlx1/2, including Olig2. Consequently, heterozygosity of Dlx1/2 and Rbbp4 leads to an increase in the production of OLIG2+ cells. These findings highlight the importance of the interplay between TFs and chromatin remodelers in regulating cell fate decisions.

2022-06-01 | GSE194076 | 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