PRDM16 regulates the postnatal fate of embryonic radial glia via VCAM1-dependent mechanisms
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA902489 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR22317144_1.fastq.gz | Fastqsanger.gz | |||
| SRR22317144_2.fastq.gz | Fastqsanger.gz | |||
| SRR22317145_1.fastq.gz | Fastqsanger.gz | |||
| SRR22317145_2.fastq.gz | Fastqsanger.gz | |||
| SRR22317146_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 14 |
Similar Datasets
Project description:Postnatally, a subpopulation of embryonic neural stem cells becomes adult neural stem cells, which primarily generate olfactory bulb interneurons in mice. Although embryonic and adult neural stem cells have been characterized, the mechanisms that regulate the transition from embryonic to adult neural stem cells remain poorly understood. We show that PR domain-containing 16 (Prdm16) promotes the transition from embryonic to adult neural stem cells. By single-cell RNA sequencing, it reveals postnatal persistence of radial glia in Prdm16 cKO mice.
2024-12-30 | GSE218159 | GEO
Project description: Not available
| S-EPMC12276310 | biostudies-literature
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
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 | GSE77697 | GEO
Project description:As the seat of our cognition, the human neocortex is an object of immense fascination. Human neocortex expansion during evolution has been attributed to an increase in the proliferative capacity of neural progenitor cells during development, particularly basal radial glia. Despite their evolutionary relevance, the genomic changes driving human basal radial glia biology remain uncharacterized. We used comparative chromatin and transcriptional profiling of neural progenitor cells isolated from gorilla, chimpanzee and human cerebral organoids to identify cis-regulatory elements that have gained activity in humans. Focusing specifically on basal radial glia, we discovered that morphoregulatory enhancer activity and gene expression signatures distinguish human basal radial glia from other great apes. Functional analysis of the morphoregulatory genes FAM107A and CNGA3 in human organoids revealed that these genes contribute to the morphological complexity of human basal radial glia. Taken together, our inter-species comparison of basal radial glia suggests that human-specific morphoregulatory signatures characterise neocortex evolution.
2026-08-04 | GSE331434 | GEO
Project description:As the seat of our cognition, the human neocortex is an object of immense fascination. Human neocortex expansion during evolution has been attributed to an increase in the proliferative capacity of neural progenitor cells during development, particularly basal radial glia. Despite their evolutionary relevance, the genomic changes driving human basal radial glia biology remain uncharacterized. We used comparative chromatin and transcriptional profiling of neural progenitor cells isolated from gorilla, chimpanzee and human cerebral organoids to identify cis-regulatory elements that have gained activity in humans. Focusing specifically on basal radial glia, we discovered that morphoregulatory enhancer activity and gene expression signatures distinguish human basal radial glia from other great apes. Functional analysis of the morphoregulatory genes FAM107A and CNGA3 in human organoids revealed that these genes contribute to the morphological complexity of human basal radial glia. Taken together, our inter-species comparison of basal radial glia suggests that human-specific morphoregulatory signatures characterise neocortex evolution.
2026-08-04 | GSE331437 | GEO
Project description:As the seat of our cognition, the human neocortex is an object of immense fascination. Human neocortex expansion during evolution has been attributed to an increase in the proliferative capacity of neural progenitor cells during development, particularly basal radial glia. Despite their evolutionary relevance, the genomic changes driving human basal radial glia biology remain uncharacterized. We used comparative chromatin and transcriptional profiling of neural progenitor cells isolated from gorilla, chimpanzee and human cerebral organoids to identify cis-regulatory elements that have gained activity in humans. Focusing specifically on basal radial glia, we discovered that morphoregulatory enhancer activity and gene expression signatures distinguish human basal radial glia from other great apes. Functional analysis of the morphoregulatory genes FAM107A and CNGA3 in human organoids revealed that these genes contribute to the morphological complexity of human basal radial glia. Taken together, our inter-species comparison of basal radial glia suggests that human-specific morphoregulatory signatures characterise neocortex evolution.
2026-08-04 | GSE331436 | GEO
Project description:As the seat of our cognition, the human neocortex is an object of immense fascination. Human neocortex expansion during evolution has been attributed to an increase in the proliferative capacity of neural progenitor cells during development, particularly basal radial glia. Despite their evolutionary relevance, the genomic changes driving human basal radial glia biology remain uncharacterized. We used comparative chromatin and transcriptional profiling of neural progenitor cells isolated from gorilla, chimpanzee and human cerebral organoids to identify cis-regulatory elements that have gained activity in humans. Focusing specifically on basal radial glia, we discovered that morphoregulatory enhancer activity and gene expression signatures distinguish human basal radial glia from other great apes. Functional analysis of the morphoregulatory genes FAM107A and CNGA3 in human organoids revealed that these genes contribute to the morphological complexity of human basal radial glia. Taken together, our inter-species comparison of basal radial glia suggests that human-specific morphoregulatory signatures characterise neocortex evolution.
2026-08-04 | GSE331435 | GEO
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
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