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Dlx1/2-Dependent Expression of Meis2 Promotes Neuronal Fate

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

PROVIDER: PRJNA779538 | ENA |

REPOSITORIES: ENA

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			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

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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

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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]

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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]

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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

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.

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Transcription Factors Dlx1 and Otp Segregate the Identity of Orexigenic/Anti-thermogenic- and Growth Promoting-Neurons in the Arcuate Nucleus

Project description:The hypothalamic arcuate nucleus contains multiple types of neurons controlling critical physiological processes. However, the gene regulatory network directing their development remains rudimentary. Here we report that two transcription factors Otp and Dlx1 segregate the identity of orexigenic/anti-thermogenic NPY/AgRP- and growth-promoting GHRH-neurons in the developing arcuate nucleus. Otp-null and Dlx1-null mice lose NPY/AgRP and GHRH expression, respectively. Dlx1-null mice also show enhanced expression of Otp/NPY/AgRP, which is normalized in Dlx1;Otp-double mutant mice. Correspondingly, Dlx1-null mice exhibit decreased growth, lower body temperature and increased feeding. Furthermore, our genome-wide studies identify Otp as a negative target gene of Dlx1. Therefore, Otp is critical for NPY/AgRP-neuronal development, while Dlx1 promotes GHRH-neuronal development and antagonizes NPY/AgRP-neuronal development. These results identify a mechanism for segregating the identity of two functionally related neurons, and the Dlx1-Otp axis likely contributes to coordinating energy balance and growth by maintaining a proper ratio of NPY/AgRP- to GHRH-neurons.

2018-05-31 | GSE104372 | GEO

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