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A Long Noncoding RNA, LncMyod, Regulates Myogenic Lineage Progression by Modulating Chromatin Accessibility

ABSTRACT: A Long Noncoding RNA, LncMyod, Regulates Myogenic Lineage Progression by Modulating Chromatin Accessibility

PROVIDER: PRJNA532654 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8890940.fastq.gz	Fastqsanger.gz
	SRR8890950.fastq.gz	Fastqsanger.gz
	SRR8892200_1.fastq.gz	Fastqsanger.gz
	SRR8892200_2.fastq.gz	Fastqsanger.gz
	SRR8890771_1.fastq.gz	Fastqsanger.gz

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A Long Noncoding RNA, LncMyod, Regulates Myogenic Lineage Progression by Modulating Chromatin Accessibility

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

2020-12-08 | GSE129768 | GEO

A long noncoding RNA, <i>LncMyoD</i>, modulates chromatin accessibility to regulate muscle stem cell myogenic lineage progression.

Project description:Epigenetics regulation plays a critical role in determining cell identity by controlling the accessibility of lineage-specific regulatory regions. In muscle stem cells, epigenetic mechanisms of how chromatin accessibility is modulated during cell fate determination are not fully understood. Here, we identified a long noncoding RNA, LncMyoD, that functions as a chromatin modulator for myogenic lineage determination and progression. The depletion of LncMyoD in muscle stem cells led to the down-regulation of myogenic genes and defects in myogenic differentiation. LncMyoD exclusively binds with MyoD and not with other myogenic regulatory factors and promotes transactivation of target genes. The mechanistic study revealed that loss of LncMyoD prevents the establishment of a permissive chromatin environment at myogenic E-box-containing regions, therefore restricting the binding of MyoD. Furthermore, the depletion of LncMyoD strongly impairs the reprogramming of fibroblasts into the myogenic lineage. Taken together, our study shows that LncMyoD associates with MyoD and promotes myogenic gene expression through modulating MyoD accessibility to chromatin, thereby regulating myogenic lineage determination and progression.

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Transcriptome sequencing analysis of LncMyod-knockdown satellite cells by RNA-seq

Project description:To understand the effect of LncMyod knockdown on cultured satellite cells, we isolated satellite cells from mouse hindlimb and cultured them in vitro with siRNA treatment targeting LncMyod. Following RNA-seq showed that loss of LncMyod leads to difficiencies in myogenic differentiation.

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Long noncoding RNA lncMREF promotes myogenic differentiation and muscle regeneration by interacting with the Smarca5/p300 complex [ChIP-seq_p300]

Project description:Long noncoding RNAs play important roles in the spatial and temporal regulation of muscle development and regeneration. Nevertheless, the determination of their biological functions and mechanisms underlying muscle satellite cell differentiation remains challenging. Here, we identified a novel lncRNA named lncMREF as a specific positive regulator of muscle regeneration in mice, pigs and humans. Functional studies demonstrated that lncMREF is significantly upregulated in activated skeletal muscle satellite cells and promotes myogenic differentiation and muscle regeneration. Mechanistically, lncMREF interacts with Smarca5 to promote chromatin remodeling and accessibility when muscle satellite cells are activated, thereby facilitating genomic binding of p300/H3K27 to upregulate the expression of myogenic regulators, such as MyoD and cell differentiation. Our results unravel a new temporal-specific epigenetic regulation during muscle regeneration and reveal that lncMREF/Smarca5-mediated epigenetic programming is responsible for muscle satellite cell differentiation, which provides new insights into the regulatory mechanism of muscle regeneration in adult animals.

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Long noncoding RNA lncMREF promotes myogenic differentiation and muscle regeneration by interacting with the Smarca5/p300 complex [ChIP-seq_H3k27ac]

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Long noncoding RNA lncMREF promotes myogenic differentiation and muscle regeneration by interacting with the Smarca5/p300 complex [ATAC-seq]

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Assessment Of Long Noncoding RNA CCAT1 In Colorectal Cancer Patients

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Long noncoding RNA lncMREF promotes myogenic differentiation and muscle regeneration by interacting with the Smarca5/p300 complex [RNA-seq]

Project description:Here, we identified a novel lncRNA named lncMREF as a specific positive regulator of muscle regeneration in mice, pigs and humans. Functional studies demonstrated that lncMREF is significantly upregulated in activated skeletal muscle satellite cells and promotes myogenic differentiation and muscle regeneration. Mechanistically, lncMREF interacts with Smarca5 to promote chromatin remodeling and accessibility when muscle satellite cells are activated, thereby facilitating genomic binding of p300/H3K27 to upregulate the expression of myogenic regulators, such as MyoD and cell differentiation. Our results unravel a new temporal-specific epigenetic regulation during muscle regeneration and reveal that lncMREF/Smarca5-mediated epigenetic programming is responsible for muscle satellite cell differentiation, which provides new insights into the regulatory mechanism of muscle regeneration in adult animals.

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Location matters – how the cytoskeletal protein Leiomodin 1 controls myogenic differentiation by modulating Sirtuin 1 localization

Project description:During myogenic differentiation the architecture and proteome of muscle stem cells undergo extensive remodelling. These processes are only partially understood and display impairments in age and disease. Using mass spectrometry to analyse protein dynamics during myogenic differentiation, we identified the actin nucleator Leiomodin 1 (LMOD1) increasing in abundance in early phases of myogenic differentiation. Knockdown of LMOD1 in primary myoblasts severely affected myogenic differentiation and fusion of myotubes, while overexpression had the opposite effect. Mechanistically, we show that LMOD1 interacts with Sirtuin1 (SIRT1) and that both follow similar changes in nuclear/cytoplasmic localization during differentiation. We demonstrate that LMOD1 influences SIRT1 localization and the expression of a subset of its target genes. Consistently, depletion or pharmacological inhibition of SIRT1 partially rescues the effects of LMOD1 knockdown. Our work identifies a novel regulator of myogenic differentiation that might be a potential target to improve muscle regeneration in aging and disease.

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