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Co-effects of m6A dynamics and chromatin accessibility changes regulate cardiomyocyte differentiation

ABSTRACT: Co-effects of m6A dynamics and chromatin accessibility changes regulate cardiomyocyte differentiation

PROVIDER: PRJNA966899 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR24415960.fastq.gz	Fastqsanger.gz
	SRR24415960_1.fastq.gz	Fastqsanger.gz
	SRR24415960_2.fastq.gz	Fastqsanger.gz
	SRR24415961.fastq.gz	Fastqsanger.gz
	SRR24415961_1.fastq.gz	Fastqsanger.gz

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Co-effects of m6A dynamics and chromatin accessibility changes regulate cardiomyocyte differentiation

Project description:The growth and differentiation of cardiomyocytes are primarily driven by gene expression dynamics, with various epigenetic modifications playing a crucial role in this process. One of the most common modifications on mRNA, m6A, influences the regulation of mRNA metabolism; however, its function remains enigmatic. In this study, we identified a correlation between m6A modification and cardiomyocyte differentiation by profiling m6A dynamics during the transition of pluripotent stem cells into cardiomyocytes. Although the overall m6A modification level remains relatively stable, most genes exhibit changes in their m6A levels as cardiomyocyte differentiation progresses. We observed that alterations in chromatin accessibility can impact the binding capabilities of m6A writers, erasers, and readers, consequently affecting m6A levels. Furthermore, the coordinated changes of m6A and chromatin accessibility are closely associated with early-stage cardiomyocyte differentiation. These findings suggest that m6A is a significant factor in determining the fate of cardiomyocyte differentiation, shedding light on its role in this critical process.

2023-08-24 | GSE231549 | GEO

Co-effects of m6A and chromatin accessibility dynamics in the regulation of cardiomyocyte differentiation.

Project description:BackgroundCardiomyocyte growth and differentiation rely on precise gene expression regulation, with epigenetic modifications emerging as key players in this intricate process. Among these modifications, N6-methyladenosine (m6A) stands out as one of the most prevalent modifications on mRNA, exerting influence over mRNA metabolism and gene expression. However, the specific function of m6A in cardiomyocyte differentiation remains poorly understood.ResultsWe investigated the relationship between m6A modification and cardiomyocyte differentiation by conducting a comprehensive profiling of m6A dynamics during the transition from pluripotent stem cells to cardiomyocytes. Our findings reveal that while the overall m6A modification level remains relatively stable, the m6A levels of individual genes undergo significant changes throughout cardiomyocyte differentiation. We discovered the correlation between alterations in chromatin accessibility and the binding capabilities of m6A writers, erasers, and readers. The changes in chromatin accessibility influence the recruitment and activity of m6A regulatory proteins, thereby impacting the levels of m6A modification on specific mRNA transcripts.ConclusionOur data demonstrate that the coordinated dynamics of m6A modification and chromatin accessibility are prominent during the cardiomyocyte differentiation.

| S-EPMC10416456 | biostudies-literature

Pathogen induced m6A dynamics regulate plant immunity

Project description:Pathogen induced m6A dynamics regulate plant immunity

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Histone modification and accessibility dynamics during human cardiomyocyte differention

Project description:Histone modification and accessibility dynamics during human cardiomyocyte differention

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Pathogen induced m6A dynamics regulate plant immunity

Project description:Post-transcriptional regulation of mRNA mediated by methylation at the N6 position of adenine (N6-methyladenosine (m6A)) can have profound effects on transcriptome regulation in plants. Focused studies across eukaryotes offer glimpses into the processes governed by m6A throughout developmental and disease states. However, we lack an understanding of the dynamics and scope of regulatory potential m6A possesses during biotic stress responses in plants. Here, we provide a comprehensive look into the effects m6A has on both the short-term and long-term response to pathogenic stress in Arabidopsis. m6A deposition influences transcript abundance and stability on populations of stress-responsive transcripts. Additionally, we demonstrate a time- and stress-dependent modulation of m6A highlighting specific stress-responsive transcripts regulated directly and indirectly by this mark. As a result, m6A deficient plants are more resistant to bacterial pathogen Pseudomonas syringae infection, and this mark is essential in dictating and coordinating transcript fate during a biotic stress reprograming event. Overall, we show m6A is a critical aspect in modulating the post-transcriptional regulation of the transcriptome in response to pathogenic stress in plants.

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m6A profile in cardiomyocytes

Project description:To determine the role of m6A methylation in the heart we isolated primary cardiomyocytes and performed m6A immunoprecipitation followed by RNA sequencing. We measured the level of m6A methylation on cardiomyocyte mRNA, and found a significant increase in response to hypertrophic stimulation, suggesting a potential role for m6A methylation in the development of cardiomyocyte hypertrophy. Analysis of m6A methylation showed significant enrichment in genes that regulate kinases and intracellular signaling pathways. Inhibition of METTL3 completely abrogated the ability of cardiomyocytes to undergo hypertrophy when stimulated to grow, while increased expression of the m6A RNA methylase METTL3 was sufficient to promote cardiomyocyte hypertrophy both in vitro and in vivo. Our study identified METTL3-mediated methylation of mRNA on N6-adenosines as a dynamic modification that is enhanced in response to hypertrophic stimuli and is necessary for a normal hypertrophic response in cardiomyocytes.

2018-08-29 | GSE119170 | GEO

Reelin and Thrombospondin1 regulate cardiomyocyte proliferation through Vldlr

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AP-1 Regulates Chromatin Accessibility to Promote Sarcomere Disassembly and Cardiomyocyte Protrusion during Zebrafish Heart Regeneration

Project description:The zebrafish has emerged as a powerful model to study cardiac regeneration; however, the mechanisms by which cardiomyocytes respond to damage by disassembling sarcomeres, proliferating, and repopulating the injured area remain unclear. Here, we show that AP-1 transcription factors play an essential role in regulating the cardiomyocyte response. Using ATAC-Seq, we first find that the cardiomyocyte chromatin accessibility landscape is dynamic following cryoinjury, and that AP-1 motifs are the most highly enriched in regions that gain accessibility during regeneration. Using a cardiomyocyte-specific dominant-negative approach, we show that AP-1 promotes cardiomyocyte proliferation as well as chromatin accessibility at genes regulating sarcomere disassembly and cardiomyocyte protrusion into the injured area. We further find distinct temporal requirements for AP-1 during cardiac regeneration. Altogether, these results indicate that AP-1 plays a key role in the cardiomyocyte response to injury by promoting chromatin accessibility changes, allowing the activation of gene expression programs that support regeneration.

2020-06-10 | GSE130940 | GEO

Mechanical forces regulate cardiomyocyte myofilament maturation via the VCL-SSH1-CFL axis

Project description:Mechanical forces regulate cell behavior and tissue morphogenesis. In particular, cardiac tissues require mechanical stimuli generated by the heartbeat for differentiation and maturation, but the molecular mechanisms underlying these processes remain unclear. Here, we first show that mechanical forces acting via the mechanosensitive factor Vinculin (VCL) are essential for cardiomyocyte myofilament maturation and that cardiac contractility regulates the localization and activation of Vinculin. To further analyze the role of Vinculin in myofilament maturation, we examined its interactome in contracting cardiomyocytes and found many cytoskeletal factors including actinins. We also identified Slingshot protein phosphatase 1 (SSH1), which we show is recruited by Vinculin to regulate F-actin rearrangement and myofilament maturation through its association with the actin depolymerizing factor Cofilin (CFL). Together, our results reveal that mechanical forces generated by cardiac contractility regulate cardiomyocyte maturation through the VCL-SSH1-CFL axis, providing mechanistic insight into how mechanical forces are transmitted intracellularly to regulate myofilament maturation.

2019-09-06 | PXD014624 | Pride

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