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ASH2L Regulates Postnatal Neurogenesis through Onecut2-mediated Inhibition of TGF-β Signaling Pathway

ABSTRACT: ASH2L Regulates Postnatal Neurogenesis through Onecut2-mediated Inhibition of TGF-β Signaling Pathway

PROVIDER: PRJNA982756 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR24894607_1.fastq.gz	Fastqsanger.gz
	SRR24894607_2.fastq.gz	Fastqsanger.gz
	SRR24894608_1.fastq.gz	Fastqsanger.gz
	SRR24894608_2.fastq.gz	Fastqsanger.gz
	SRR24894609_1.fastq.gz	Fastqsanger.gz

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ASH2L Regulates Postnatal Neurogenesis through Onecut2-mediated Inhibition of TGF-β Signaling Pathway

Project description:We applied whole transcriptome analysis of P7 NSPCs from WT/Ash2l-iKO mice to gain insight into genes that might be dysregulated and transcriptionally different after Ash2l deletion.

2023-06-20 | GSE234685 | GEO

ASH2L regulates postnatal neurogenesis through Onecut2-mediated inhibition of TGF-β signaling pathway.

Project description:The ability of neural stem/progenitor cells (NSPCs) to proliferate and differentiate is required through different stages of neurogenesis. Disturbance in the regulation of neurogenesis causes many neurological diseases, such as intellectual disability, autism, and schizophrenia. However, the intrinsic mechanisms of this regulation in neurogenesis remain poorly understood. Here, we report that Ash2l (Absent, small or homeotic discs-like 2), one core component of a multimeric histone methyltransferase complex, is essential for NSPC fate determination during postnatal neurogenesis. Deletion of Ash2l in NSPCs impairs their capacity for proliferation and differentiation, leading to simplified dendritic arbors in adult-born hippocampal neurons and deficits in cognitive abilities. RNA sequencing data reveal that Ash2l primarily regulates cell fate specification and neuron commitment. Furthermore, we identified Onecut2, a major downstream target of ASH2L characterized by bivalent histone modifications, and demonstrated that constitutive expression of Onecut2 restores defective proliferation and differentiation of NSPCs in adult Ash2l-deficient mice. Importantly, we identified that Onecut2 modulates TGF-β signaling in NSPCs and that treatment with a TGF-β inhibitor rectifies the phenotype of Ash2l-deficient NSPCs. Collectively, our findings reveal the ASH2L-Onecut2-TGF-β signaling axis that mediates postnatal neurogenesis to maintain proper forebrain function.

| S-EPMC10406892 | biostudies-literature

Meningeal cells contribute to postnatal cortical neurogenesis.

Project description:Postnatal brain neurogenesis in mammals is believed to be restricted to rare germinative remnants of the neuroepithelium. In this study, we discovered that, in the postnatal brain, a subset of embryonically derived progenitors is present in meningeal substructures. These cells migrate from the meningeal substructures to the retrosplenial and visual motor cortex and differentiate into (electrically) functional integrated neurons. Lineage tracing analysis revealed that this subset of neural progenitors originate largely from PDGFR+ cells. PDGFR-derived cells differentiate mostly into Satb2+ neurons in cortical layers I-IV. Thus, a reservoir of embryonically derived progenitors in the meninges contributes to postnatal cerebral cortical neurogenesis.

2016-11-23 | E-MTAB-4951 | biostudies-arrayexpress

Meningeal cells contribute to postnatal cortical neurogenesis.

Project description:Meningeal cells contribute to postnatal cortical neurogenesis.

| PRJEB14890 | ENA

The KMT2 complex protein ASH2L controls meiosis through silencing transposon

Project description:Meiosis is precisely controlled by complex gene expression programs and involves epigenetic reprogramming and silencing of transposable elements. ASH2L (Absent, small or homeotic 2-like) is a core component of KMT2 complexes conferring H3K4 trimethylation, and plays key roles in mouse embryonic development, neurogenesis, and liver function. However, its role in meiosis remains elusive. Here, we demonstrate an essential role of Ash2l for meiosis. Using a germ cell-specific Ash2l knockout mouse model, we found that Ash2l deficiency leads to meiotic arrest and sterility in both sexes. Ash2l-deficient spermatocytes exhibit failures in chromosomal synapsis, blockades in meiotic recombination, and increased apoptosis. Mechanistically, we found that the Ash2l deficiency results in a global loss of H3K4me3 in promoter regions and significantly decreases expression of thousands of genes, including those for H3K9 di-methylation, DNA methylation and transposon repression, crucial for meiotic prophase I progression. Furthermore, we observed that Ash2l mutant spermatocytes display hypomethylation at transposon sites and ectopic expression of LINE1-ORF1P. Our findings thus reveal a previously unappreciated role of the ASH2L-dependent H3K4me3 modification and provide clues to the molecular mechanisms in epigenetic disorders underlying male infertility.

2024-10-19 | GSE246296 | GEO

Atr maintains chromosomal integrity during postnatal cerebellar neurogenesis

Project description:Atr maintains chromosomal integrity during postnatal cerebellar neurogenesis

| PRJNA338316 | ENA

COMPASS Family Histone Methyltransferase ASH2L Mediates Corticogenesis via Transcriptional Regulation of Wnt Signaling [ChIP-seq]

Project description:We show that the COMPASS family histone methyltransferase co-factor ASH2L is required in NPCs proliferation and upper layer cortical projection neurons production and position. Deletion of ASH2L impairs trimethylation of H3K4 and transcriptional machinery specifically for subsets of Wnt-β-catenin signaling, disrupting their transcription and consequently inhibiting the proliferation ability of NPCs in late stages of neurogenesis.

2019-07-16 | GSE120987 | GEO

COMPASS Family Histone Methyltransferase ASH2L Mediates Corticogenesis via Transcriptional Regulation of Wnt Signaling [RNA-seq]

2019-07-16 | GSE120986 | GEO

COMPASS Family Histone Methyltransferase ASH2L Mediates Corticogenesis via Transcriptional Regulation of Wnt Signaling [RNA-Seq 2]

2019-07-16 | GSE133413 | GEO

COMPASS Family Histone Methyltransferase ASH2L Mediates Corticogenesis via Transcriptional Regulation of Wnt Signaling

Project description:This SuperSeries is composed of the SubSeries listed below Histone methylation is essential for regulating gene expression during organogenesis to maintain stem cells and execute a proper differentiation program for their descendants. Here, we show that the COMPASS family histone methyltransferase co-factor ASH2L is required for maintaining neural progenitor cells (NPCs) and the production and positioning of projection neurons during neocortex development. Specifically, loss of ASH2L in NPCs results in malformation of the neocortex; the mutant neocortex shows fewer neurons that are also abnormal in composition and laminar position. Moreover, ASH2L loss impairs the trimethylation of H3K4 and the transcriptional machinery specific for Wnt-β-catenin signaling, inhibiting the proliferation ability of NPCs at late stages of neurogenesis by disrupting S phase entry to inhibit cell cycle progression. Overexpressing β-catenin after ASH2L elimination rescues the proliferation deficiency. Therefore, our findings demonstrate ASH2L is crucial for modulating Wnt signaling to maintain NPCs and generate a full complement of neurons during mammalian neocortex development.

2019-07-16 | GSE120988 | GEO

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