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LSD1 Corepressor Rcor2 Orchestrates Neurogenesis in the Developing Mouse Brain

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus

PROVIDER: GSE75040 | GEO | 2016/01/22

SECONDARY ACCESSION(S): PRJNA302273

REPOSITORIES: GEO

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LSD1 co-repressor Rcor2 orchestrates neurogenesis in the developing mouse brain.

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.

| S-EPMC4736047 | biostudies-literature

LSD1 Corepressor Rcor2 Orchestrates Neurogenesis in the Developing Mouse Brain [ChIP-Seq]

Project description:ChIP-seq analysis using Flag M2, LSD1 and H3K4me2 antibodies respectively in Rcor2Flag embryonic brain.

2016-01-22 | GSE75039 | GEO

LSD1 Corepressor Rcor2 Orchestrates Neurogenesis in the Developing Mouse Brain [RNA-Seq]

Project description:RNA-seq analysis of Rcor2fl/fl and Rcor2cko embryonic cortex.

2016-01-22 | GSE75038 | GEO

LSD1 Corepressor Rcor2 Orchestrates Neurogenesis in the Developing Mouse Brain

Project description:LSD1 Corepressor Rcor2 Orchestrates Neurogenesis in the Developing Mouse Brain

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LSD1-RCOR2 binding and LSD1 and BRD9 transcriptome analysis in Merkel cell carcinoma cells

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

2020-02-16 | GSE124864 | GEO

Mitotic WNT signalling orchestrates neurogenesis in the developing neocortex

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.

| S-SCDT-EMBOJ-2021-108041 | biostudies-other

Mitotic WNT signalling orchestrates neurogenesis in the developing neocortex.

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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Snip1 and PRC2 coordinate the intrinsic apoptosis, cell division, and neurogenesis in the developing brain

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

2023-07-12 | GSE212445 | GEO

Mouse neurogenesis

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

2021-12-31 | GSE167050 | GEO

REST corepressors RCOR1 and RCOR2 and the repressor INSM1 regulate the proliferation-differentiation balance in the developing brain.

Project description:The transcriptional events that lead to the cessation of neural proliferation, and therefore enable the production of proper numbers of differentiated neurons and glia, are still largely uncharacterized. Here, we report that the transcription factor Insulinoma-associated 1 (INSM1) forms complexes with RE1 Silencing Transcription factor (REST) corepressors RCOR1 and RCOR2 in progenitors in embryonic mouse brain. Mice lacking both RCOR1 and RCOR2 in developing brain die perinatally and generate an abnormally high number of neural progenitors at the expense of differentiated neurons and oligodendrocyte precursor cells. In addition, Rcor1/2 deletion detrimentally affects complex morphological processes such as closure of the interganglionic sulcus. We find that INSM1, a transcription factor that induces cell-cycle arrest, is coexpressed with RCOR1/2 in a subset of neural progenitors and forms complexes with RCOR1/2 in embryonic brain. Further, the Insm1-/- mouse phenocopies predominant brain phenotypes of the Rcor1/2 knockout. A large number of genes are concordantly misregulated in both knockout genotypes, and a majority of the down-regulated genes are targets of REST. Rest transcripts are up-regulated in both knockouts, and reducing transcripts to control levels in the Rcor1/2 knockout partially rescues the defect in interganglionic sulcus closure. Our findings indicate that an INSM1/RCOR1/2 complex controls the balance of proliferation and differentiation during brain development.

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