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Characterization of the role of SETDB1 in Muscle stem cells during skeletal muscle regeneration [ChIP-seq]

ABSTRACT: Characterization of the role of SETDB1 in Muscle stem cells during skeletal muscle regeneration [ChIP-seq]

PROVIDER: PRJNA1065801 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR27701114_1.fastq.gz	Fastqsanger.gz
	SRR27701114_2.fastq.gz	Fastqsanger.gz
	SRR27701115_1.fastq.gz	Fastqsanger.gz
	SRR27701115_2.fastq.gz	Fastqsanger.gz
	SRR27701116_1.fastq.gz	Fastqsanger.gz

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Characterization of the role of SETDB1 in Muscle stem cells during skeletal muscle regeneration [RNA-seq]

Project description:Muscle regeneration is process where different type of cells are interacting together to ensure a proper muscle regeneration. As Muscle stem cells are the central protagonist of muscle regeneration, we performed single cell RNA-seq to observe the change between the different cell types when SETDB1 is absent in Muscle stem cells. Muscle Stem Cells were isolated from the conditional mice model Setdb1-cKO and were isolated by Fluorescence-activated cell sorting (FACS).

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Project description:The histone 3 lysine 9 (H3K9)-specific methyltransferase (KMT) Setdb1 is essential for both stem cell pluripotency and terminal differentiation of different cell types. To shed light on Setdb1 role(s) in these mutually exclusive processes, we used mouse skeletal myoblasts as a model of terminal differentiation. Ex vivo studies on isolated single myofibres showed that Setdb1 is required for muscle adult stem cells expansion following activation and in vitro studies on skeletal myoblasts confirmed that Setdb1 suppresses terminal myoblast differentiation. We used genome-wide analyses to identify Setdb1 direct target genes in myoblasts and observed a release of Setdb1 from the promoter of selected target genes upon myoblast terminal differentiation, concomitant to a nuclear export of Setdb1 to the cytoplasm. We demonstrated that both genomic release and cytoplasmic Setdb1 relocalisation during differentiation were dependent on canonical Wnt signalling. Taken together, our findings uncover a functional link between Setdb1 and canonical Wnt signalling in skeletal muscle cells, which affects the expression of a subset of Setdb1 target genes. We revealed Wnt-dependent subcellular relocalisation of Setdb1 as a novel mechanism regulating Setdb1 functions. ChIP-seq of Setdb1 and H3K9me3 in Myoblast cells (C2C12)

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