LSD1 Corepressor Rcor2 Orchestrates Neurogenesis in the Developing Mouse Brain [RNA-Seq]
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE75038 | GEO | 2016/01/22
SECONDARY ACCESSION(S): PRJNA302276
REPOSITORIES: GEO
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Project description:ChIP-seq analysis using Flag M2, LSD1 and H3K4me2 antibodies respectively in Rcor2Flag embryonic brain.
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Project description:Epigenetic regulatory complexes play key roles in the modulation of transcriptional regulation underlying neural stem cell (NSC) proliferation and progeny specification. How specific cofactors guide histone demethylase LSD1/KDM1A complex to regulate distinct NSC-related gene activation and repression in cortical neurogenesis remains unclear. Here we demonstrate that Rcor2, a co-repressor of LSD1, is mainly expressed in the central nervous system (CNS) and plays a key role in epigenetic regulation of cortical development. Depletion of Rcor2 results in reduced NPC proliferation, neuron population, neocortex thickness and brain size. We find that Rcor2 directly targets Dlx2 and Shh, and represses their expressions in developing neocortex. In addition, inhibition of Shh signals rescues the neurogenesis defects caused by Rcor2 depletion both in vivo and in vitro. Hence, our findings suggest that co-repressor Rcor2 is critical for cortical development by repressing Shh signalling pathway in dorsal telencephalon.
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Project description:This SuperSeries is composed of the SubSeries listed below.
2016-01-22 | GSE75040 | GEO
Project description:LSD1 Corepressor Rcor2 Orchestrates Neurogenesis in the Developing Mouse Brain
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Project description:This project consists in 3 datasets: - Samples from adult mouse brains (Hippocampus, Cortex and Cerebellum): Cul3 +/- or +/+; 5 animals per condition. - Samples from embryonic mouse cortex: either Cul3 +/- or +/+ - Samples from embryonic mouse cortex: Cul3 fl/fl Emx-1-Cre ("hom"); Cul3 +/fl Emx1-Cre ("het") or Cul3+/fl ("control")
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Project description:Purpose:To gain futher insight into how endothelial Arid1a regulates the angiogenesis, neurogenesis, and astrogenesis,RNA-seq was used to analyze the genome-wide changes resulting from isolated endothelial cells of E15 Arid1a endothelial conditional knockout mice and littermate wild-type. Methods: mRNA from E15 isolated endothelial cells of Arid1afl/fl and Arid1acKO-Tie2 mice was extracted. Specifically, Agilent 2100 Bioanalyze was used to quality controlled and quantified. then, mRNA was converted to cDNA and bound the library. RNA-sequencing analysis was used by the Illumina HiSeq 2500 platform in Annoroad Genomics. Results: Approximately one six thousand transcripts showed differential expression between the Arid1afl/fl and Arid1acKO-Tie2 mice brain cortex, with a fold change ≥2 and p value <0.05.Geneontology analysis of the up-regulated genes showed obvious enrichment of biological processes related to development process and regulation of cell communication.The down-regulated genes exhibited enrichment of biological processes related to cell movement. These results reflected endothelial Arid1a plays a vital role in cortex development. Conclusions: Endothelial Arid1a RNA-seq would provide a overall understanding how endothelial Arid1a regulates the Balance among angiogenesis, neurogenesis, and astrogenesis in the developing Brain
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Project description:The role of WNT/β-catenin signalling in mouse neocortex development remains ambiguous. Most studies demonstrate that WNT/β-catenin regulates progenitor self-renewal but others suggest it can also promote differentiation. Here we explore the role of WNT/STOP signalling, which stabilizes proteins during G2/M by inhibiting glycogen synthase kinase (GSK3)-mediated protein degradation. We show that mice mutant for cyclin Y and cyclin Y-like 1 (Ccny/l1), key regulators of WNT/STOP signalling, display reduced neurogenesis in the developing neocortex. Specifically, basal progenitors, which exhibit delayed cell-cycle progression, were drastically decreased. Ccny/l1-deficient apical progenitors show reduced asymmetric division due to an increase in apical-basal astral microtubules. We identify the neurogenic transcription factors Sox4 and Sox11 as direct GSK3 targets that are stabilized by WNT/STOP signalling in basal progenitors during mitosis and that promote neuron generation. Our work reveals that WNT/STOP signalling drives cortical neurogenesis and identifies mitosis as a critical phase for neural progenitor fate.
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Project description:The role of WNT/β-catenin signalling in mouse neocortex development remains ambiguous. Most studies demonstrate that WNT/β-catenin regulates progenitor self-renewal but others suggest it can also promote differentiation. Here we explore the role of WNT/STOP signalling, which stabilizes proteins during G2/M by inhibiting glycogen synthase kinase (GSK3)-mediated protein degradation. We show that mice mutant for cyclin Y and cyclin Y-like 1 (Ccny/l1), key regulators of WNT/STOP signalling, display reduced neurogenesis in the developing neocortex. Specifically, basal progenitors, which exhibit delayed cell cycle progression, were drastically decreased. Ccny/l1-deficient apical progenitors show reduced asymmetric division due to an increase in apical-basal astral microtubules. We identify the neurogenic transcription factors Sox4 and Sox11 as direct GSK3 targets that are stabilized by WNT/STOP signalling in basal progenitors during mitosis and that promote neuron generation. Our work reveals that WNT/STOP signalling drives cortical neurogenesis and identifies mitosis as a critical phase for neural progenitor fate.
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Project description:Purpose: To gain futher insight into how GSDMD regulates the proliferative of neural progenitors ,RNA-seq was used to analyze the genome-wide changes resulting from the cerebral cortices of E13 GSDMD conditional knock out mice and littermate wild-type. Methods: Total RNA from E13 telencephalic tissue of wild-type(WT) and Gsdmdfl/fl;Nestin-Cre mice was extracted. Specifically, Agilent 2100 Bioanalyze was used to quality controlled and quantified. then, total RNA was converted to cDNA and bound the library. RNA-sequencing analysis was used by the Illumina HiSeq 2500 platform in Annoroad Genomics Results: Approximately one thousand transcripts showed differential expression between the wild-type(WT) and Gsdmdfl/fl;Nestin-Cre mice brain cortex, with a fold change ≥1.5 and p value <0.05.Geneontology analysis of the up-regulated genes showed obvious enrichment of biological processes related to development and proliferation.The down-regulated genes exhibited enrichment of biological processes related to the negative regulation of cell proliferation and developmental process. These results reflected GSDMD plays a role in cortex development. Conclusions: RNA-seq based transcriptome characterization would provide a overall understanding how GSDMD gene contribute to brain cortical development.
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Project description:Purpose:To gain a deeper insight into how PRDM16 regulates neuron-vascular communication for angiogenesis, RNA-sequencing (RNA-seq) was performed to analyze the genome-wide changes by PRDM16 deletion at E15. Methods: Total RNA was extracted from E15 telencephalic tissue of Prdm16cKO and Prdm16fl/fl mice. Then total RNA was quality controlled and quantified using an Agilent 2100 Bioanalyzer. After converting to cDNA and building library, high-throughput sequencing was performed using the Illumina HiSeq 2500 platform in Annoroad Genomics. Results: Approximately approximately one thousand transcripts showed differential expression between the Prdm16fl/fl and Prdm16cKO brain cortex, with a fold change ≥1.5 and p value <0.05. Gene ontology (GO) analysis showed that the down-regulated genes were enriched in the terms related to neurogenesis, blood vessel development and secretion by cells. Up-regulated genes showed a significant enrichment of terms involved in negative regulation of cell communication and negative regulation of angiogenesis. These results reflected the importance of PRDM16 in cortical development. Conclusions: We conclude that RNA-seq based transcriptome characterization would provide a framework for understanding how Prdm16 gene contribute to brain cortical development.
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