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ChIP-seq profiling of myogenin and p300 occupancy in the context of rexinoid signaling during early myogenic differentiation

ABSTRACT: ChIP-seq profiling of myogenin and p300 occupancy in the context of rexinoid signaling during early myogenic differentiation

PROVIDER: PRJNA587703 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10401160.fastq.gz	Fastqsanger.gz
	SRR10401161.fastq.gz	Fastqsanger.gz
	SRR10401162.fastq.gz	Fastqsanger.gz
	SRR10401163.fastq.gz	Fastqsanger.gz
	SRR10401164.fastq.gz	Fastqsanger.gz

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ChIP-seq profiling of myogenin and p300 occupancy in the context of rexinoid signaling during early myogenic differentiation

Project description:Deciphering the molecular mechanisms underpinning myoblast differentiation is a critical step in developing the best strategy to promote muscle regeneration in patients suffering from muscle-related diseases. We have previously established that a rexinoid x receptor (RXR)-selective agonist enhances the differentiation and fusion of myoblasts through a direct regulation of MyoD expression, coupled with an augmentation of myogenin protein. Here, we found that RXR signaling modifies the chromatin state distribution of myogenin, promoting the binding preference of myogenin for poised enhancers and a distinct motif. We also found an association of myogenin with rexinoid-responsive gene expression and identified an epigenetic signature related to histone acetyltransferase p300. Moreover, RXR signaling instigates residue-specific histone acetylation at enhancers co-occupied by p300 and myogenin. Thus, genomic distribution of transcriptional regulators is an important designate for identifying novel targets as well as developing therapeutics that modulate epigenetic landscape in a selective manner to promote muscle regeneration.

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Project description:While skeletal myogenesis is tightly coordinated by myogenic regulatory factors including MyoD and myogenin, chromatin modifications have emerged as vital mechanisms of myogenic regulation. We have previously established that bexarotene, a clinically approved agonist of retinoid X receptor, promotes the specification and differentiation of skeletal muscle lineage. Here, we examine a genome-wide impact of rexinoids on myogenic differentiation through integral RNA-seq and ChIP-seq analyses. We found that bexarotene promotes myoblast differentiation through the coordination of exit from the cell cycle and the activation of muscle-related genes. We uncovered a new mechanism of rexinoid action which is mediated by the nuclear receptor and largely reconciled through a direct regulation of MyoD gene expression. In addition, we determined a rexinoid-responsive residue-specific histone acetylation at a distinct chromatin state associated to MyoD and myogenin. Thus, we provide novel molecular insights into the interplay between retinoid X receptor signaling and chromatin states pertinent to myogenic programs in early myoblast differentiation.

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Project description:Molecular regulation of stem cell differentiation is exerted through both genetic and epigenetic determinants over distal regulatory or enhancer regions. Understanding the mechanistic action of active or poised enhancers is thus imperative for control of stem cell differentiation. Based on a genome-wide co-occurrence of different epigenetic marks in committed proliferating myoblasts, we have previously generated a 14-state chromatin state model to profile residue-specific histone acetylation in early myoblast differentiation. Here, we use genome-wide chromatin state association to delineate the functional mode of transcription regulators in early myogenic differentiation. We define a role of transcriptional coactivator p300, when recruited by master muscle regulator MyoD, in the establishment and regulation of myogenic loci at the onset of terminal differentiation. In addition, we reveal an enrichment of residue- and loci-specific histone acetylation at p300 associated active or poised enhancers, particularly when enlisted by MyoD. We provide novel molecular insights into the regulation of myogenic enhancers by p300 in concert with MyoD. Our studies present a valuable aptitude for driving stage specific chromatin state or enhancers pharmacologically to treat muscle related diseases and for the identification of additional myogenic targets and molecular interactions for therapeutic development.

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ChIP-seq profiling of transcriptional co-activator p300 during early myogenic differentiation

Project description:ChIP-seq profiling of transcriptional co-activator p300 during early myogenic differentiation

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