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Heart tube morphogenesis is regulated by segment-specific gene regulatory networks controlled by MEF2C [snATAC-seq]

ABSTRACT: Heart tube morphogenesis is regulated by segment-specific gene regulatory networks controlled by MEF2C [snATAC-seq]

PROVIDER: PRJNA1179365 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR31147507_1.fastq.gz	Fastqsanger.gz
	SRR31147507_2.fastq.gz	Fastqsanger.gz
	SRR31147508_1.fastq.gz	Fastqsanger.gz
	SRR31147508_2.fastq.gz	Fastqsanger.gz
	SRR31147509_1.fastq.gz	Fastqsanger.gz

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Similar Datasets

Heart tube morphogenesis is regulated by segment-specific gene regulatory networks controlled by MEF2C [snATAC-seq]

Project description:The transcription factor MEF2C plays a critical role in the development of the linear heart tube, but the specific transcriptional networks controlled by MEF2C remain largely undefined. To address this, we performed combined single-nucleus RNA- and ATAC- sequencing on wild type and MEF2C-null embryos at distinct stages of development. We identified a broadly “posteriorized” cardiac gene signature and chromatin landscape throughout the heart tube in the absence of MEF2C. By integrating our gene expression and chromatin accessibility data in a deep-learning based model, we were able to construct developmental trajectories for each of the outflow tract, ventricular, and inflow tract lineages and determined how each of these segment-specific trajectories were distinctly altered in the MEF2C-null embryos. We computationally identified potential segment-specific MEF2C-dependent enhancers. Using transgenesis in zebrafish embryos, we identified novel MEF2C-dependent enhancers with activity in the developing heart tube from among these candidates. Finally, using inferred gene regulatory networks we discovered a genetic interaction between MEF2C and the atrial nuclear hormone receptor NR2F2, revealing that the MEF2C-null heart malformations are partly driven by a transcriptional network with increased NR2F2 activity. These studies not only provide a rich description of the genomic regulation of early heart tube development, but provide a generalizable framework for using genetic mutants to dissect the transcriptional networks that govern developmental processes.

2024-11-04 | GSE280538 | GEO

Heart tube morphogenesis is regulated by segment-specific gene regulatory networks controlled by MEF2C [snRNA-Seq]

2024-11-04 | GSE280543 | GEO

Heart tube morphogenesis is regulated by segment-specific gene regulatory networks controlled by MEF2C

Project description:Heart tube morphogenesis is regulated by segment-specific gene regulatory networks controlled by MEF2C

| PRJNA1179451 | ENA

Heart tube morphogenesis is regulated by segment-specific gene regulatory networks controlled by MEF2C [snRNA-Seq]

Project description:Heart tube morphogenesis is regulated by segment-specific gene regulatory networks controlled by MEF2C [snRNA-Seq]

| PRJNA1179369 | ENA

Heart tube morphogenesis is regulated by segment-specific gene regulatory networks controlled by MEF2C

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

2024-11-04 | GSE280587 | GEO

MEF2C hypofunction in neuronal and neuroimmune populations produces MEF2C haploinsufficiency syndrome behaviors in mice

Project description:Microdeletions of the MEF2C gene are linked to a syndromic form of autism termed MEF2C haploinsufficiency syndrome (MCHS). Here, we show that MCHS-associated missense mutations cluster in the conserved DNA binding domain and disrupt MEF2C DNA binding. DNA binding-deficient global Mef2c heterozygous mice (Mef2c-Het) display numerous MCHS-like behaviors, including autism-related behaviors, as well as deficits in cortical excitatory synaptic transmission. We find that hundreds of genes are dysregulated in Mef2c-Het cortex, including significant enrichments of autism risk and excitatory neuron genes. In addition, we observe an enrichment of upregulated microglial genes, but not due to neuroinflammation in the Mef2c-Het cortex. Importantly, conditional Mef2c heterozygosity in forebrain excitatory neurons reproduces a subset of the Mef2c-Het phenotypes, while conditional Mef2c heterozygosity in microglia reproduces social deficits and repetitive behavior. Together our findings suggest that MEF2C regulates typical brain development and function through multiple cell types, including excitatory neuronal and neuroimmune populations.

2020-10-24 | GSE139419 | GEO

Role of MEF2C in the Endothelial Cells Derived from Human Induced Pluripotent Stem Cells

Project description:Human induced pluripotent stem cells (hiPSCs) not only provide an abundant source of vascular cells for potential therapeutic applications in vascular disease but also constitute an excellent model for understanding the mechanisms that regulate the differentiation and the functionality of vascular cells. Here, we reported that myocyte enhancer factor 2C (MEF2C) transcription factor, but not any other members of the MEF2 family, was robustly upregulated during the differentiation of vascular progenitors and endothelial cells (ECs) from hiPSCs. Vascular endothelial growth factors (VEGF) strongly induced MEF2C expression in endothelial lineage cells. The specific upregulation of MEF2C during the commitment of endothelial lineage was dependent on the extracellular signal regulated kinase (ERK). Moreover, knockdown of MEF2C with shRNA in hiPSCs did not affect the differentiation of ECs from these hiPSCs, but greatly reduced the migration and tube formation capacity of the hiPSC-derived ECs. Through a chromatin immunoprecipitation-sequencing, genome-wide RNA-sequencing, quantitative RT-PCR, and immunostaining analyses of the hiPSC-derived endothelial lineage cells with MEF2C inhibition or knockdown compared to control hiPSC-ECs, we identified TNF-related apoptosis inducing ligand (TRAIL) and transmembrane protein 100 (TMEM100) as novel targets of MEF2C. This study demonstrates an important role for MEF2C in regulating human EC functions and highlights MEF2C and its downstream effectors as potential targets to treat vascular malfunction-associated diseases.

2024-01-01 | GSE222083 | GEO

MEF2C phosphorylation is required for chemotherapy resistance in acute myeloid leukemia [mutant MEF2C]

Project description:In acute myeloid leukemia, chemotherapy resistance remains prevalent and poorly understood. Using functional proteomics of patient AML specimens, we identified MEF2C S222 phosphorylation as a specific marker of primary chemoresistance. We found that transgenic Mef2cS222A/S222A mice engineered to block MEF2C phosphorylation exhibited normal hematopoiesis, but were resistant to leukemogenesis induced by MLL-AF9. MEF2C phosphorylation was required for leukemia stem cell maintenance, induced by MARK kinases in cells, and blocked by selective MARK inhibitor MRT199665, which caused apoptosis of MEF2C-activated human AML cell lines and primary patient specimens, but not those lacking MEF2C. These findings identify signaling-dependent dysregulation of transcription factor control as a determinant of therapy response in AML, with immediate potential for improved diagnosis and therapy for this disease.

2018-07-23 | GSE94453 | GEO

Expression data from HUVEC adenovirally overexpressing MEF2C

Project description:The transcription factor MEF2C is specifically induced by VEGF in endothelial cells. To delineate target genes of MEF2C in endothelial cells, which might be important during angiogenesis also, MEF2C was overexpressed adenovirally in human umbilical vein endothelial cells (HUVECs) over a period of 8 to 32 hours. Expression data should be compared to control infected cells, to discriminate against virally induced genes, and should be further compared to HUVECs infected with an adenovirus encoding for a dominant-negative form of MEF2. HUVECs of the same batch, passage 3 were infected with Ad.con, Ad.MEF2C or Ad.DNMEF2 for 8, 16 or 32 hours for RNA extraction and hybridization on Affymetrix microarrays.

2013-06-01 | E-GEOD-46279 | biostudies-arrayexpress

Genome-wide maps of MEF2C and H3K27ac localization in HUVECs

Project description:MEF2C is one of the substantially expressed transcriptional factors in endothelial cells, but its genomic localization is unknown. This time, we established a new antibody for MEF2C, and performed ChIP-seq to identify MEF2C binding site in whole genome manner. H3K27Ac binding sites were also detected in the same way. We used chromatin immunoprecipitation with deep sequencing (ChIP-seq) of HUVECs treated with or without pitavastatin for 4hours, we identified MEF2C and H3K27Ac binding regions.HUVECs were used within the first 6 passages. For MEF2C studies, HUVECs were cultivated in medium EGM2MV containing pitavastatin at a concentration of 1 ?M, and same concentration of DMSO was used as a control sample. For H3K27ac, HUVECs were starved for 16 hours and harvested without statin treatment.

2013-01-01 | E-GEOD-32644 | biostudies-arrayexpress

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