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PRDM16 regulates a temporal transcriptional program to promote progression of cortical neural progenitors

ABSTRACT: PRDM16 regulates a temporal transcriptional program to promote progression of cortical neural progenitors

PROVIDER: PRJNA683596 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13218651_1.fastq.gz	Fastqsanger.gz
	SRR13218651_2.fastq.gz	Fastqsanger.gz
	SRR13218652_1.fastq.gz	Fastqsanger.gz
	SRR13218652_2.fastq.gz	Fastqsanger.gz
	SRR13218653_1.fastq.gz	Fastqsanger.gz

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PRDM16 regulates a temporal transcriptional program to promote progression of cortical neural progenitors

Project description:Radial glia (RG) in the neocortex sequentially generate distinct subtypes of projection neurons, accounting for the diversity and complex assembly of cortical neural circuits. Mechanisms that drive the rapid and precise temporal progression of RG are beginning to be elucidated. Here we reveal that the RG-specific transcriptional regulator PRDM16 promotes the transition of early to late phase of neurogenesis in the mouse neocortex. Loss of Prdm16 delays the timely progression of RG, leading to defective cortical laminar organization. Our genomic analyses demonstrate that PRDM16 regulates a subset of genes that are dynamically expressed between early and late neurogenesis. We show that PRDM16 suppresses target gene expression through limiting chromatin accessibility of permissive enhancers. We further confirm that critical target genes regulated by PRDM16 comprise neuronal specification genes, cell cycle regulators and molecules required for neuronal migration. These findings provide evidences to support that neural progenitors temporally shift gene expression program to achieve neural cell diversity.

2021-03-03 | GSE162854 | GEO

PRDM16 regulates a temporal transcriptional program to promote progression of cortical neural progenitors.

Project description:Radial glia (RG) in the neocortex sequentially generate distinct subtypes of projection neurons, accounting for the diversity and complex assembly of cortical neural circuits. Mechanisms that drive the rapid and precise temporal progression of RG are beginning to be elucidated. Here, we reveal that the RG-specific transcriptional regulator PRDM16 promotes the transition of early to late phase of neurogenesis in the mouse neocortex. Loss of Prdm16 delays the timely progression of RG, leading to defective cortical laminar organization. Our genomic analyses demonstrate that PRDM16 regulates a subset of genes that are dynamically expressed between early and late neurogenesis. We show that PRDM16 suppresses target gene expression through limiting chromatin accessibility of permissive enhancers. We further confirm that crucial target genes regulated by PRDM16 are neuronal specification genes, cell cycle regulators and molecules required for neuronal migration. These findings provide evidence to support the finding that neural progenitors temporally shift the gene expression program to achieve neural cell diversity.

| S-EPMC7990860 | biostudies-literature

RNA-Seq of E14 MGE, Prdm16 WT vs cKO

Project description:This study aimed to understand the role of the transcriptional regulator Prdm16 in the development of cortical interneurons in the mouse. Prdm16 was knocked out in cells derived from the medial ganglionic eminence (MGE) by using an Nkx2.1-Cre driver line in combination with a line carrying floxed Prdm16 alleles and with a Cre-dependent tdTomato reporter line (Ai14). The sequencing data compares the gene expression profiles of dissected MGEs at embryonic day 14 (E14), a stage when cortical interneurons are being generated from MGE progenitors.

2020-10-22 | GSE159728 | GEO

A shared temporal program for ventral spinal cord progenitors [CaTS-RNA]

Project description:A shared temporal program for ventral spinal cord progenitors [CaTS-RNA]

| PRJNA1101107 | ENA

Role of Prdm16 in fibro-adipogenic progenitors

Project description:Role of Prdm16 in fibro-adipogenic progenitors

| PRJNA624179 | ENA

Transcriptome profiling of WT and Prdm16 mutant cells in embryonic mouse cerebral cortex.

Project description:Transcriptome profiling of radial glia, intermediate progenitors, and cortical neurons in WT and Prdm16 conditional knock-out (cKO) mouse (Emx1Ires-Cre; Prdm16flox/flox) at embryonic day 15.5.

2018-06-21 | GSE111660 | 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

RNA-seq analysis of Wildtype and Prdm16 cKO ventricular zone tissue during cortex development in mouse

Project description:Purpose: To explore the mechanisms by which PRDM16 regulates reactive oxygen species levels and oxidative stress in radial glia progenitors during cortical development in mouse.

2020-02-16 | GSE142684 | GEO

A shared temporal chromatin program for ventral spinal cord progenitors [CaTS-ATAC]

Project description:A shared temporal chromatin program for ventral spinal cord progenitors [CaTS-ATAC]

| PRJNA1103700 | ENA

Changes in DNA methylation upon gain and loss of Prdm16 function

Project description:Cortical neurogenesis requires the fine tuning of gene expression, modulated by genetic and epigenetic mechanisms during the entire process. Among the epigenetic factors expressed by the proliferative radial glia cells, Prdm16 has been shown to play a key role in cell proliferation. We found Prdm16 to be expressed exclusively by radial glia cells and to be rapidly turned off in newborn neurons. Predictably, Prdm16-null mice displayed a decrease in cortical thickness as a consequence of an impairment in self-renewal of radial glia cells. Conversely, Prdm16-overexpressing neural progenitors showed an increase in self-renewal activity and failed to complete differentiation. Lineage restriction in differentiating stem cells is achieved by chromatin modifications such as histone modifications and DNA methylation along the promoters of stemness-related genes. We found the expression of the DNA methyltransferase Dnmt3b to be inversely correlated to that of Prdm16. Loss and gain of Prdm16 function leaded to an up- and down-regulation of Dnmt3b, respectively. Functional analysis confirmed Prdm16 competence to repress Dnmt3b expression. Finally, IUE of Prdm16 together with Dnmt3b rescued the increase in radial glia cells self-renewal observed with Prdm16 alone. Thus, Prdm16 may play a crucial role in ensuring neural progenitor self-renewal, mainly through the maintenance of the unmethylated state of stemness-related genes.

2022-05-25 | GSE59574 | GEO

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