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

ORGANISM(S): Mus musculus

PROVIDER: GSE188602 | GEO | 2021/11/13

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

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 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 [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

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

| PRJNA779538 | ENA

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

Dlx1/2-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

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 and Dlx2 control neuronal versus oligodendroglial cell fate acquisition in the developing forebrain.

Project description:Progenitors within the ventral telencephalon can generate GABAergic neurons and oligodendrocytes, but regulation of the neuron-glial switch is poorly understood. We investigated the combinatorial expression and function of Dlx1&2, Olig2, and Mash1 transcription factors in the ventral telencephalon. We show that Dlx homeobox transcription factors, required for GABAergic interneuron production, repress oligodendrocyte precursor cell (OPC) formation by acting on a common progenitor to determine neuronal versus oligodendroglial cell fate acquisition. We demonstrate that Dlx1&2 negatively regulate Olig2-dependant OPC formation and that Mash1 promotes OPC formation by restricting the number of Dlx+ progenitors. Progenitors transplanted from Dlx1&2 mutant ventral telencephalon into newborn wild-type mice do not produce neurons but differentiate into myelinating oligodendrocytes that survive into adulthood. Our results identify another role for Dlx genes as modulators of neuron versus oligodendrocyte development in the ventral embryonic forebrain.

| S-EPMC2039927 | biostudies-literature

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

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