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PRDM16 is required for proper specification of the working ventricular myocardium by suppressing alternative cardiomyocyte cell fates.

ABSTRACT: PRDM16 is required for proper specification of the working ventricular myocardium by suppressing alternative cardiomyocyte cell fates.

PROVIDER: PRJNA1074780 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR27922974_1.fastq.gz	Fastqsanger.gz
	SRR27922974_2.fastq.gz	Fastqsanger.gz
	SRR27922975_1.fastq.gz	Fastqsanger.gz
	SRR27922975_2.fastq.gz	Fastqsanger.gz
	SRR27922976.fastq.gz	Fastqsanger.gz

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Similar Datasets

PRDM16 is required for proper specification of the working ventricular myocardium by suppressing alternative cardiomyocyte cell fates.

Project description:PRDM16 is a transcription factor with histone methyltransferase activity expressed at the earliest stages of cardiac development. Pathogenic mutations in humans lead to cardiomyopathy, conduction abnormalities and heart failure. PRDM16 is specifically expressed in ventricular but not atrial cardiomyocytes and declines in expression postnatally. Since in other tissues PRDM16 is best known for its role in binary cell fate decisions, we hypothesized a similar decision-making function in cardiomyocytes. Here, we demonstrated that cardiomyocyte-specific deletion of Prdm16 during cardiac development results in contractile dysfunction and abnormal electrophysiology of the postnatal heart, resulting in premature death. By combined RNA+ATAC single-cell sequencing we found that PRDM16 favors ventricular working cardiomyocyte identity, by opposing the activity of master regulators of atrial and ventricular conduction fate. Myocardial loss of Prdm16 during development resulted in hyperplasia of the ventricular conduction system. Hence, PRDM16 plays an indispensable role during cardiac development by driving ventricular working cardiomyocyte identity.

2024-09-18 | GSE255382 | GEO

PRDM16 Functions as A Compact Myocardium-Enriched Transcription Factor Required to Maintain Compact Myocardial Cardiomyocyte Identity in Left Ventricle (scRNA-seq)

Project description:The loss of compact myocardial cardiomyocyte (compact CM) identity suggests that PRDM16 deficiency may dramatically alter the cellular composition in left ventricular (LV) compact myocardium. To test this hypothesis, we performed single-cell RNA-seq (scRNA-seq) to examine gene dysreulation in Prdm16cKO heart. We also performed Visium Spatial Transcriptomics (ST) to facilitate mapping CM clusters to their original locations in the heart. As a result, we were able to demonstrate gene misregulation in Prdm16cKO mouse mainly occurred in LV compact CM.

2021-12-20 | GSE179390 | GEO

PRDM16 Functions as A Compact Myocardium-Enriched Transcription Factor Required to Maintain Compact Myocardial Cardiomyocyte Identity in Left Ventricle (Spatial Transcriptomics)

2021-12-20 | GSE179392 | GEO

Prdm16 Knockout Brown Adipose Tissue

Project description:Gene expression profile from brown adipose tissues of Prdm16 knockout and wile type mice. Prdm16 is a transcription factor that regulates the thermogenic gene program in brown and beige adipocytes. However, whether Prdm16 is required for the development or physiological function of brown adipose tissue (BAT) in vivo has been unclear. By analyzing mice that selectively lacked Prdm16 in the brown adipose lineage, we found that Prdm16 was dispensable for embryonic BAT development. Brown adipose tissues were collected from Prdm16 knockout and wiletype mice with 4 biological replicates per condition. Experiment was done in two separate batch for 6-week-old and 11-month-old. Extracted RNA was hybridized to Agilent two-color arrays.

2014-04-09 | E-GEOD-55080 | biostudies-arrayexpress

Prdm16 mutation determines sex-specific cardiac metabolism and identifies two novel cardiac metabolic regulators

Project description:Mutation of the PRDM16 gene causes human dilated and noncompaction cardiomyopathy. The PRDM16 protein is a transcriptional regulator that affects cardiac development via Tbx5 and Hand1, thus regulating myocardial structure. The biallelic inactivation of Prdm16 induces severe cardiac dysfunction with postnatal lethality and hypertrophy in mice. The early pathological events that occur upon Prdm16 inactivation have not been explored. This study performed in-depth pathophysiological and molecular analyses of male and female Prdm16csp1/wt mice that carry systemic, monoallelic Prdm16 gene inactivation. We systematically assessed early molecular changes through transcriptomics, proteomics, and metabolomics. Kinetic modelling of cardiac metabolism was performed in silico with CARDIOKIN.

2023-07-21 | PXD043601 | Pride

Australian Working Kelpie

Project description:Australian Working Kelpie (WGS)

| PRJEB53208 | ENA

Cistromic and epigenomic changes in Prdm16 knock-out brown adipose tissue

Project description:Prdm16 is a transcription factor that drives a complete program of brown adipocyte differentiation, but the mechanism by which Prdm16 activates gene transcription remains unknown. Utilizing ChIP-seq teqhnique, we found that Prdm16 binds to chromatin at/near many brown fat-selective genes in BAT. Interestingly, Prdm16-deficiency dramatically reduced the binding of Med1 to Prdm16-target sites. Indeed, Prdm16 binds and recruits Med1 to BAT-enriched genes and the loss of Prdm16 caused a fundamental change in chromatin architecture at key BAT-selective genes and also reduced transcirptional activity. Moreover, Prdm16, through its interaction with Med1, defines and regulates the activity of super-enhancers that drive the expression of cell identity genes. Together, these data demonstrate that Prdm16 drives gene transcription by recruiting Med1 to control chromatin architecture and super-enhancers. Brown adipose tissues were collected from Prdm16 knockout and wiletype 9-month-old mice and ChIP-seq was performed for Prdm16, PolII, Med1, and H3K27ac.

2015-02-10 | E-GEOD-63965 | biostudies-arrayexpress

mRNA expression of murine hematopoietic stem cells and ex vivo murine MLL-AF9 cells deficient for total PRDM16 or f-PRDM16, and AF9 cells overexpressing individual PRDM16 isoforms

Project description:Group 1 -- WT or PRDM16-KO ex vivo murine MLL-AF9 cells, and PRDM16-KO AF9 cells overexpressing either f-PRDM16 or s-PRDM16. Group 2 -- WT or total PRDM16-KO murine HSCs isolated from adult BM. Group 3 -- WT or total PRDM16-KO murine HSCs isolated from fetal liver. Group 4 -- WT or f-PRDM16-KO murine HSCs (expressing s-PRDM16 only) isolated from fetal liver.

2018-06-08 | GSE112860 | GEO

PRDM16 ChIP-Seq in Prdm16 WT and KO duodenal crypts

Project description:PRDM16 ChIP was perfomed in control and Prdm16 KO crypts isolated from the duodenum of 6 week old mice 3 days after inducible gene deletion

2020-02-26 | GSE131487 | GEO

Histone methyltransferase PRDM16 in tumor suppression

Project description:PRDM16 is highly enriched in adult stem cells and plays a crucial role in multiple developmental processes. Here we demonstrate that PRDM16 is a histone H3K4 methyltransferase and this activity is essential for PRDM16 to function as a tumor suppressor. We show that PRDM16, through its regulation of transcription factor GFI1b, antagonizes the functions of MLL fusion proteins by repressing HOXA gene expression and therefore, specifically suppresses the transformation capability of MLL-AF9, MLL-AF6 and MLL-ENL. Furthermore, overexpression of PRDM16, but not the inactive PRDM16 mutant, blocks MLL mediated leukemogenesis while PRDM16 depletion significantly shortens the disease latency in vivo. We also show that PRDM16 activity is dynamically required at the pre-leukemic stage, but not in fully transformed leukemia, depicting a little known sequence of events necessary for clonal expansion during cancer evolution. Given the importance of PRDM16 and the loss of PRDM16 methyltransferase activity in an array of human malignancies, our findings provide broad insights for PRDM16-dependent physiological and pathological processes.

2016-12-15 | GSE64218 | GEO

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