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

ABSTRACT: 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

ORGANISM(S): Mus musculus

PROVIDER: GSE182335 | GEO | 2021/08/19

REPOSITORIES: GEO

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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

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

2021-11-13 | GSE188602 | GEO

Transcription Factors Dlx1/2 Are Required for Making All Interneurons in the Olfactory Bulb [Dlx1/2]

Project description:Purpose: To assess changes in gene expression profiles from the E16.5 wild type littermate controls LGE and Dlx1/2-/- mutant mice LGE (lateral ganglionic eminence). Methods: Total RNA was isolated and sequenced using an Illumina Hi-seq 2500. Raw data was analyzed using TopHat. Genes were considered significantly changed which perform fold-change>=2 and P value <= 0.05. Results: Compared to controls, 804 genes were significantly down regulated, and 673 genes were up regulated in the RNA expression level of the mutant LGE.

2019-01-25 | GSE121214 | GEO

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

Transcriptomic analysis from lateral ganglionic eminence (LGE) of control and Isl1 conditional knock-out (cKO) mice.

Project description:RNA-seq analysis was used to identify genes that are differentially expressed between control and Isl1 cKO LGEs.

2022-03-13 | GSE198385 | 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

Dlx1/2-Dependent Expression of Meis2 Promotes Neuronal Fate

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

| PRJNA779538 | ENA

Transcriptome of wildtype and Meis2 mutant in the developing palate

Project description:We use RNA-sequencing to profile the different expression genes in the palatal mesenchyme of wildtype and Wnt1Cre;Meis2f/f mice at E12.5. 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 | GSE143912 | GEO

Identification of gene targets of Meis2

Project description:The homeodomain protein Meis1 is essential for definitive hematopoiesis and vascular patterning in the mouse embryo. Meis2, another member of the same family, shares 82% protein identities with Meis1. Our present study suggested Meis2 exerts two distinguishable effects in differentiating ES cells. First, it increases the numbers of hematopoietic progenitors and extends their persistence in culture. Second, Meis2 skews hematopoietic differentiation by suppressing erythroid while enhancing megakaryocytic progenitor differentiation. To identify the underlying transcriptional bases of these actions, we carried out microarray analysis to compare the various populations of cells developing in ES differentiation cultures in the presence and absence of Meis2 induction. ES cells with dox-inducible Meis2 (A2lox.Meis2) were differentiated as embryoid bodies (EBs) for 6 days before plating on OP9-GFP cell monolayers and cytokines, and treated with (+) or without (-) doxycycline (dox). Cells were purified by cell sorting on day 7 or 8 into various populations based on levels of CD41 expression: GFP-CD41-, GFP-CD41+ (day 7) and GFP-CD41-,GFP-CD41int, and GFP-CD41hi (day 8). Gene expression of these purified populations was determined by microarray analysis.

2012-08-02 | E-GEOD-34541 | biostudies-arrayexpress

MEIS2 is a novel oncogenic partner in AML1-ETO positive AML [RNA-Seq mouse]

Project description:MEIS2 collaborates with AML1-ETO in inducing acute myeloid leukemia in a murine bone marrow transplantation model We employed RNA-seq to assess similarities/differences among murine leukemic bone marrow samples transduced with either AML1-ETO/Meis2, AML1-ETO9a/Meis2, or AML1-ETO9a

2016-07-04 | E-GEOD-81329 | biostudies-arrayexpress

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