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Compared with the Mock group, FGF8+10 treatment mature the differentiated LPM-like cells to form LM-like cells, and gene expression profile at single cell level of Msx1+ mesenchymal progenitors from mouse E10.5 embryos

ABSTRACT: Compared with the Mock group, FGF8+10 treatment mature the differentiated LPM-like cells to form LM-like cells, and gene expression profile at single cell level of Msx1+ mesenchymal progenitors from mouse E10.5 embryos

PROVIDER: PRJNA972755 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR24575412_1.fastq.gz	Fastqsanger.gz
	SRR24575412_2.fastq.gz	Fastqsanger.gz
	SRR24575413_1.fastq.gz	Fastqsanger.gz
	SRR24575413_2.fastq.gz	Fastqsanger.gz
	SRR24575414_1.fastq.gz	Fastqsanger.gz

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Compared with the Mock group, FGF8+10 treatment mature the differentiated LPM-like cells to form LM-like cells [RNA-seq]

Project description:When treated with FGF8+10, LM makers were upregulated and the expression levels were higher than that of the Mock cells.

2024-03-20 | GSE232584 | GEO

Compared with the Mock group, FGF8+10 treatment mature the differentiated LPM-like cells to form LM-like cells [RNA-seq]

Project description:Compared with the Mock group, FGF8+10 treatment mature the differentiated LPM-like cells to form LM-like cells [RNA-seq]

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Compared with the Mock group, FGF8+10 treatment mature the differentiated LPM-like cells to form LM-like cells, and gene expression profile at single cell level of Msx1+ mesenchymal progenitors from mouse E10.5 embryos

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

2024-03-20 | GSE232586 | GEO

Janibacter sp. LM strain:LM

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Gene expression profile at single cell level of Msx1+ mesenchymal progenitors from mouse E10.5 embryos [scRNA-seq]

Project description:Gene expression profile at single cell level of Msx1+ mesenchymal progenitors from mouse E10.5 embryos [scRNA-seq]

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Global quantitative proteomics analysis reveals the downstream signaling networks of Msx1 and Msx2 in skeletal muscle development

Project description:The homeoprotein Msx1 and Msx2 involved in normal skeletal muscle development and also contribute to muscle defects if altered during development. Deciphering the downstream signaling networks of Msx1 and Msx2 in myoblasts differentiation will help us to understand the molecular events that contribute to muscle defects. The objective of this study was to evaluate the proteomics characteristics in Msx1 and Msx2 mediated myoblasts differentiation, using isobaric tags for the relative and absolute quantification labelling technique (iTRAQ). The results showed that 1535 proteins with quantitative information were obtained. Volcano plots illustrated, in undifferentiated stage, 32 common downstream regulatory proteins for Msx1 and Msx2, 39 specific regulatory proteins for Msx1, and 13 specific for Msx2. While, in differentiated stage, 17 common downstream regulatory proteins for Msx1 and Msx2, 10 specific regulatory proteins for Msx1, and 21 specific for Msx2. Gene ontology, KEGG pathway and protein-protein interaction networks analyses revealed these proteins primarily associated with Arginine and proline metabolism, Glycolysis/Gluconeogenesis, Fatty acid degradation, Metabolism of xenobiotics by cytochrome P450 and Apoptosis. In addition, our data shows Acta1 was probably a core of the downstream regulatory networks of Msx1 and Msx2 in skeletal muscle development. The findings will help us to understand the molecular roles of Msx1 and Msx2 during muscle development as well as regeneration, and to understand the molecular events that contribute to muscle defects.

2023-07-20 | PXD026944 | Pride

MSX1-induced neural crest-like phenotype in human melanocytes

Project description:Msh homeobox 1 (MSX1) is a transcription factor implicated in neural crest specification. Ectopic expression of MSX1 reprograms mature melanocytes into a neural crest-like state as a single factor. MSX1-reprogrammed melanocytes lose pigmentation and become multipotent. To identify immediate targets of MSX1, we generated a tetracycline-inducible system (Tet-ON) in order to express MSX1 in primary melanocytes (iMSX1) in a clean and rapid way starting at defined time points and perform a global gene expression analysis.

2016-09-30 | GSE56957 | GEO

PRMT1-methylated MSX1 phase separates to control palate development

Project description:Little is known about the regulation and function of liquid‒liquid phase separation (LLPS) in craniofacial developmental disorders, where Msh homeobox 1 (MSX1) and protein arginine methyltransferase 1 (PRMT1) are two important regulators. MSX1 mutations are associated with human cleft palate, the most common craniofacial birth defect. Here, we show that MSX1 LLPS, regulated by PRMT1-catalyzed methylation, is a vertebrate-conserved mechanism underlying the proliferation of embryonic palatal mesenchymal cells (EPMs) and palatal fusion. MSX1 LLPS is triggered by its N-terminal intrinsically disordered protein region (IDR) and regulated by PRMT1-catalyzed methylation, specifically asymmetric dimethylation of arginine (R). Biochemically, PRMT1 methylates MSX1 by dimethylating the residues R150 and R157 in the MSX1 IDR. Physiochemically, the R157 to serine (R157S) mutant, R150S mutant, and hypomethylated MSX1 under PRMT1 deficiency consistently cause abnormal MSX1 LLPS to form less dynamic gel-like condensates. PRMT1 and its methylation target R residues in MSX1 are conserved in vertebrates, from zebrafish to humans. Phenotypically, less dynamic gel-like condensates formed by abnormal MSX1 LLPS cause EPM proliferation defects and cleft palate.In this study, rna-seq was used to reveal the differences between the effects of Msx1 and its mutants on hepm cells. Our findings provide a new paradigm for further exploration of LLPS underlying genetic disorders for future innovation of genetic disorder treatment by direct modulation of LLPS.

2025-01-07 | GSE285740 | GEO

LM resistance

Project description:The combination therapy of the Artemisinin-derivative Artemether (ART) with Lumefantrine (LM) (Coartem®) is an important malaria treatment regimen in many endemic countries. Resistance to Artemisinin has already been reported, and it is feared that LM resistance (LMR) could also evolve quickly. Therefore molecular markers which can be used to track Coartem®efficacy are urgently needed. Often, stable resistance arises from initial, unstable phenotypes that can be identified in vitro. Here we have used the Plasmodium falciparum multidrug resistant reference strain V1S to induce LMR in vitro by culturing the parasite under continuous drug pressure for 16 months. The initial IC50 (inhibitory concentration that kills 50% of the parasite population) was 24 nM. The resulting resistant strain V1SLM, obtained after culture for an estimated 166 cycles under LM pressure, grew steadily in 378 nM of LM; this corresponds to 15 times the IC50 of the parental strain. However, after two weeks of culturing V1SLM in drug-free medium, the IC50 returned to that of the initial, parental strain V1S. This transient drug tolerance was associated with major changes in gene expression profiles: when we explored V1SLM using the PFSANGER Affymetrix custom array, we identified 184 differentially expressed (DE) genes; amongst those 18 putative transporters including the multidrug resistance gene (pfmdr1), the multidrug resistance associated protein (pfmrp1) and the V-type H+ pumping pyrophosphatase 2 (pfvp2). Moreover, our results showed significant enrichment of genes associated with fatty acid metabolism and a clear selective advantage for two genomic loci in parasites grown under LM drug pressure, suggesting these genes may contribute to LM response in P. falciparum and could prove useful as molecular markers to monitor LM susceptibility.

2011-04-01 | E-TABM-1101 | biostudies-arrayexpress

Msx1 ChIP-Seq from C2C12 murine myoblast cells expressing Flag-Msx1 protein

Project description:The spatial and temporal control of gene expression during development requires the concerted actions of sequence-specific transcriptional regulators and epigenetic chromatin modifiers, which are thought to function within precise nuclear compartments. However, how these activities are coordinated within the dynamic context of the nuclear environment is still largely unresolved. Here we show that transcriptional repression by the Msx1 homeoprotein coordinates recruitment of Polycomb to genomic targets with localization to the nuclear periphery. We used genome-wide ChIP-Seq analyses to identify genomic binding sites for Msx1 in C2C12 murine myoblast cells.

2011-08-17 | GSE26711 | GEO

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