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Transcriptome analysis of mouse primitive heart with Dgcr8 deletion

ABSTRACT: Transcriptome analysis of mouse primitive heart with Dgcr8 deletion

PROVIDER: PRJNA379283 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR5345510_1.fastq.gz	Fastqsanger.gz
	SRR5345510_2.fastq.gz	Fastqsanger.gz
	SRR5345511_1.fastq.gz	Fastqsanger.gz
	SRR5345511_2.fastq.gz	Fastqsanger.gz
	SRR5345512_1.fastq.gz	Fastqsanger.gz

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Transcriptome analysis of mouse primitive heart with Dgcr8 deletion

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Next Generation Sequencing Analysis of gene expression profile in E9.5 Mesp1Cre/+/Dgcr8-/- embryonic heart cells transfected with NC miRNA and miR-541 mimics

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Project description:DiGeorge syndrome critical region 8 (DGCR8) is a critical component of the canonical microprocessor complex for microRNA biogenesis. However, the non-canonical functions of DGCR8 have not been studied. Here, we demonstrate that DGCR8 plays an important role in maintaining heterochromatin organization and attenuating aging. An N-terminal-truncated version of DGCR8 (DR8dex2) accelerated senescence in human mesenchymal stem cells (hMSCs) independent of its miRNA-processing activity, which is mediated by its C-terminal domains. Further studies revealed that DGCR8 maintained heterochromatin organization by interacting with the nuclear envelope protein Lamin B1, and heterochromatin-associated proteins, KAP1 and HP1 Overexpression of any of these proteins, including DGCR8, reversed premature senescent phenotypes in DR8dex2 hMSCs. Finally, DGCR8 was downregulated in pathologically and naturally aged hMSCs, whereas DGCR8 overexpression alleviated hMSC aging and osteoarthritis in mice. Taken together, these analyses uncovered a novel, miRNA processing-independent role for DGCR8 in maintaining heterochromatin organization and attenuating senescence. DGCR8 may therefore represent a new therapeutic target for alleviating human aging-related disorders.

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