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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

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

2018-09-12 | GSE96648 | GEO

Dgcr8 function in the anterior second heart field

Project description:Morphogenesis of the heart is a complex process that relies on the precise gene expression and gene expression regulators during embryonic development. Dgcr8 is a gene involved in cardiac morphogenesis and it is in the chromosomal region deleted in 22q11.2DS patients. In order to study Dgcr8 function on heart development, we inactivated this gene in the cardiac progenitor cells of mouse embryos and did expression profiling of the long RNAs and miRNAs. We used microarrays to detail the global programme of gene expression downstream of DGCR8 underlying cardiac development.

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Dgcr8 function in the anterior second heart field

Project description:Dgcr8 function in the anterior second heart field

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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

Project description:Purpose: To compare the E9.5 Dgcr8 conditional knockout embryonic heart cells transfected with NC miRNA and miR-541 mimics Methods: In vitro cultured E9.5 Dgcr8 conditional KO heart cells transfected with miR-541-5p and NC miRNA were extracted with TRIZOL 48hrs after transfection, and 10ng total RNA was reverse transcribed and amplified by Smart-seq2 protocol as described (Picelli et al., 2014). Duplicated biological samples were analyzed using Illumina HiSeqX10, Clean reads were mapped to mouse genome (mm9) using BWA software. Results: Genes differentially expressed in E9.5 Dgcr8 cKO embryonic heart cells transfected with NC miRNA and miR-541 were identified. Conclusions: miRNA-541 significantly changes the gene expression profiles of E9.5 Dgcr8 cKO embryonic heart cells and promote the cardiac function

2018-09-12 | GSE96647 | GEO

Dgcr8 deletion in the primitive heart uncovered novel microRNA regulating the balance of cardiac-vascular gene program.

Project description:Primitive mammalian heart transforms from a single tube to a four-chambered muscular organ during a short developmental window. We found that knocking out global microRNA by deleting Dgcr8 microprocessor in Mesp1 cardiovascular progenitor cells lead to the formation of extremely dilated and enlarged heart due to defective cardiomyocyte (CM) differentiation. Transcriptome analysis revealed unusual upregulation of vascular gene expression in Dgcr8 cKO hearts. Single cell RNA sequencing study further confirmed the increase of angiogenesis genes in single Dgcr8 cKO CM. We also performed global microRNA profiling of E9.5 heart for the first time, and identified that miR-541 was transiently highly expressed in E9.5 hearts. Interestingly, introducing miR-541 back into microRNA-free CMs partially rescued their defects, downregulated angiogenesis genes and significantly upregulated cardiac genes. Moreover, miR-541 can target Ctgf and inhibit endothelial function. Our results suggest that microRNAs are required to suppress abnormal angiogenesis gene program to maintain CM differentiation.

| S-EPMC6468043 | biostudies-literature

Stabilizing Heterochromatin by DGCR8 Alleviates Senescence and Osteoarthritis

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.

2019-05-28 | PXD013856 | Pride

Next Generation Sequencing Analysis of gene expression profile in Dgcr8 conditional KO embryonic hearts

Project description:Purpose: To compare the transcriptome of wild type and Mesp1Cre+/Dgcr8-/- embryonic heart at embryonic stage E8.5 and E9.5 Methods: For mRNA analysis of embryonic heart during development, total RNA of E8.5 and E9.5 heart were extracted with TRIZOL, and 100ng total RNA was reverse transcribed and amplified by Smart-seq 2 protocol as described (Picelli et al., 2014). Duplicated biological samples were analyzed using Illumina HiSeq2500, Clean reads were mapped to mouse genome (mm9) using BWA software. Results: Genes significantly differentially expressed in the CKO cardiac tube at E9.5 compared with wild type were identified. Conclusions: Dgcr8 CKO caused important gene expression changes in E9.5 embryonic heart tube

2018-09-12 | GSE96646 | GEO

MicroRNA-independent functions of DGCR8 are critically required for neocortical development and TBR1 expression

Project description:Recent evidence indicates that DROSHA, DGCR8 and DICER exert non-overlapping functions, including miRNA-independent regulatory mechanisms. It is currently unknown whether miRNA-independent functions of DGCR8 play any role in corticogenesis. Here, by phenotypic comparison of conditional knockout cortices for Dgcr8 and Dicer, we uncover that Dgcr8 deletion, in contrast to Dicer, leads to premature differentiation of neural progenitor cells and overproduction of Tbr1 positive neurons. Remarkably, miRNA depletion does not account for these phenotypic differences, indicating that miRNA-independent functions of DGCR8 are critical for corticogenesis. We propose Tbr1 transcript, bearing evolutionary conserved hairpins that resemble miRNA precursors, as one of DGCR8 targets. Our study uncovers, for the first time in the nervous system, an earlier and stronger phenotype occurring in Dgcr8 compared to Dicer mutant and proposes that this effect is mediated by miRNA-independent functions of DGCR8.

2017-02-17 | GSE82069 | GEO

MicroRNA expression profile in Dgcr8-homozygous mutant mouse embryonic stem cells

Project description:We investigated the effect of Dgcr8-homozygous mutation on microRNA expression profile in mouse embryonic stem cells. MicroRNA expression was substantially impaired, indicating a pivotal role of DGCR8 in microRNA biogenesis.

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MicroRNA expression profile in Dgcr8-homozygous mutant mouse embryonic stem cells

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