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

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

PROVIDER: PRJNA755886 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR15305449_1.fastq.gz	Fastqsanger.gz
	SRR15305449_2.fastq.gz	Fastqsanger.gz
	SRR15305450_1.fastq.gz	Fastqsanger.gz
	SRR15305450_2.fastq.gz	Fastqsanger.gz
	SRR15305451_1.fastq.gz	Fastqsanger.gz

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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

Dlx1/2-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: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

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

2021-11-13 | GSE188602 | GEO

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

Meis2 ChIP-seq in palate

Project description:ChIP-Sequencing on Meis2-HA in E12.5 palate, to identify Meis2 binding chromatin regions and target genes. Haploinsufficiency of MEIS2 is associated with cleft palate in humans and Meis2 inactivation leads to abnormal palate development in mice, implicating an essential role for Meis2 in palate development. However, its functional mechanisms remain unknown. In this study, we found widespread Meis2 expression in the developing palate in mice. Meis2 inactivation by Wnt1Cre in cranial neural crest cells led to the cleft of the secondary palate. Importantly, about half of Wnt1Cre;Meis2f/f mice exhibited submucous cleft, providing an excellent model for studying palatal bone formation and patterning. Consistent with a complete absence of the palatal bones, integrative analyses of Meis2 ChIP-seq, RNA-seq, and ATAC-seq results identified key osteogenic genes that are regulated directly by Meis2, indicating the fundamental role of Meis2 in palatal osteogenesis. De novo motif analysis discovered that the Meis2-bound regions possess highly enriched binding motifs of several key osteogenic transcription factors particularly Shox2. Comparison of Meis2 and Shox2 ChIP-seq analyses further revealed a genome-wide co-occupancy, in addition to their co-localization in the developing palate and physical interaction, suggesting that Shox2 and Meis2 act as partners. However, while Shox2 is required for proper palatal bone formation and is a direct downstream target of Meis2, Shox2 overexpression failed to rescue the palatal bone defects in Meis2 mutant background. These results, together with the facts that Meis2 expression is associated with high osteogenic potential and is required for the chromatin accessibility of osteogenic genes, support a vital function of Meis2 in setting up the ground state for palatal osteogenesis.

2020-03-23 | GSE143911 | GEO

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