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The active form of Mef2c promotes maturation of induced cardiomyocytes with p300 in direct cardiac reprogramming

ABSTRACT: The active form of Mef2c promotes maturation of induced cardiomyocytes with p300 in direct cardiac reprogramming

PROVIDER: PRJNA804194 | ENA |

REPOSITORIES: ENA

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The active form of Mef2c promotes maturation of induced cardiomyocytes with p300 in direct cardiac reprogramming

Project description:Direct cardiac reprogramming converts fibroblasts into induced cardiomyocytes (iCMs) with the minimal combination of transcription factors, Gata4 (G), Mef2c (M), and Tbx5 (T). However, the induction of functional mature iCMs is inefficient and the mechanisms remain elusive. Mef2c is a central transcription factor in direct cardiac reprogramming. We investigated the effect of Mef2c isoforms(M1, M2, M6) and transcriptional activity (M2TAD) on cardiac reprogramming on cardiac reprogramming. Then, we found that the active form of Mef2c evoked epigenetic remodeling cooperating with p300 and promoted the maturation of iCMs.

2023-06-13 | GSE196293 | GEO

Mef2c/p300 Promotes Maturation of Induced Cardiomyocytes

Project description:Mef2c/p300 Promotes Maturation of Induced Cardiomyocytes

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The active form of Mef2c promotes maturation of induced cardiomyocytes

Project description:The active form of Mef2c promotes maturation of induced cardiomyocytes

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Mef2c/p300 Promotes Maturation of Induced Cardiomyocytes

Project description:Cardiac transcription factors (TFs) directly reprogram fibroblasts into induced cardiomyocytes (iCMs), where Mef2c acts as a pioneer factor with Gata4 and Tbx5 (GT). However, generation of functional and mature iCMs is inefficient and molecular mechanisms underlying this process remains largely unknown. Here we found that transduction of transcriptionally activated Mef2c via fusion of the powerful MyoD transactivation domain increased generation of beating iCMs by 30-fold in combination with GT.

2023-06-13 | GSE222869 | GEO

P19 embryonic carcinoma (EC) cells induced to form cardiomyocytes in vitro

Project description:SAGE identification of differentiation responsive genes in P19 embryonic cells induced to form cardiomyocytes in vitro. P19 embryonic carcinoma (EC) cells, induced to form cardiomyocytes in vitro - undifferentiated cells, day 3+0.5 and day 3+3.0 of differentiation protocol. Keywords = EC cells, P19, differentiation, cardiomyocytes Keywords: time-course

2002-07-18 | E-GEOD-42 | biostudies-arrayexpress

The active form of Mef2c promotes maturation of induced cardiomyocytes

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

2023-06-13 | GSE222870 | GEO

MEF2C/p300-mediated epigenetic remodeling promotes the maturation of induced cardiomyocytes.

Project description:Cardiac transcription factors (TFs) directly reprogram fibroblasts into induced cardiomyocytes (iCMs), where MEF2C acts as a pioneer factor with GATA4 and TBX5 (GT). However, the generation of functional and mature iCMs is inefficient, and the molecular mechanisms underlying this process remain largely unknown. Here, we found that the overexpression of transcriptionally activated MEF2C via fusion of the powerful MYOD transactivation domain combined with GT increased the generation of beating iCMs by 30-fold. Activated MEF2C with GT generated iCMs that were transcriptionally, structurally, and functionally more mature than those generated by native MEF2C with GT. Mechanistically, activated MEF2C recruited p300 and multiple cardiogenic TFs to cardiac loci to induce chromatin remodeling. In contrast, p300 inhibition suppressed cardiac gene expression, inhibited iCM maturation, and decreased the beating iCM numbers. Splicing isoforms of MEF2C with similar transcriptional activities did not promote functional iCM generation. Thus, MEF2C/p300-mediated epigenetic remodeling promotes iCM maturation.

| S-EPMC10277823 | biostudies-literature

P19 embryonic carcinoma (EC) cells induced to form cardiomyocytes in vitro

2002-07-18 | GSE42 | GEO

Single-cell RNA-sequencing reveals the role of p300/CBP in calcium handing ability of prepubertal RV cardiomyocytes.

Project description:The expression of genes is determined by the openness and accessibility of chromatin, which is the most basic phenomenon in the field of life sciences.The histone acetylase p300/CBP (CBP and P300 have similar structures and functions) can catalyze the acetylation of the lysine at the 27th position of histone H3(H3K27ac), which changes the the openness and accessibility of chromatin. Thus, p300/CBP are considered to be two of the most important transcription co-factors. To further understanding the role of p300/CBP in regulating calcium handing of prepubertal RV CMs, we first detected its expression in the prepubertal RV.The expressions of p300/CBP in the prepubertal dysfunctional RV were significantly downregulated, consistent with the data of p300-ChIP-seq, which showing the loss of p300 chromatin occupancy in calcium handing genes. Then we knocked out p300/CBP in neonatal mouse. p300/CBP knockout cardiomyocytes showed a impaired calcium handing ability, similar to that in prepubertal dysfunctional RV cardiomyocytes. These results confirmed the role of p300 in regulating the calcium handing ability of prepubertal RV CMs.

2024-08-16 | GSE242193 | 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

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