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Chromatin remodeling BAF155 subunit regulates the genesis of basal progenitors in developing cortex

ABSTRACT: Chromatin remodeling BAF155 subunit regulates the genesis of basal progenitors in developing cortex

PROVIDER: PRJNA471092 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR7153360.fastq.gz	Fastqsanger.gz
	SRR7153361.fastq.gz	Fastqsanger.gz
	SRR7153362.fastq.gz	Fastqsanger.gz
	SRR7153363.fastq.gz	Fastqsanger.gz
	SRR7153364.fastq.gz	Fastqsanger.gz

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Chromatin remodeling BAF155 subunit regulates the genesis of basal progenitors in developing cortex

Project description:We have analyzed gene expression differences between control, BAF155 conditional knockout (cKO) and Pax6 cKO embryonic cortices at E15.5.

2018-05-11 | GSE114351 | GEO

Chromatin Remodeling BAF155 Subunit Regulates the Genesis of Basal Progenitors in Developing Cortex.

Project description:The abundance of basal progenitors (BPs), basal radial glia progenitors (bRGs) and basal intermediate progenitors (bIPs), in primate brain has been correlated to the high degree of cortical folding. Here we examined the role of BAF155, a subunit of the chromatin remodeling BAF complex, in generation of cortical progenitor heterogeneity. The conditional deletion of BAF155 led to diminished bIP pool and increased number of bRGs, due to delamination of apical RGs. We found that BAF155 is required for normal activity of neurogenic transcription factor PAX6, thus controlling the expression of genes that are involved in bIP specification, cell-cell interaction, and establishment of adherens junction. In a PAX6-dependent manner, BAF155 regulates the expression of the CDC42 effector protein CEP4, thereby controlling progenitor delamination. Furthermore, BAF155-dependent chromatin remodeling seems to exert a specific role in the genesis of BPs through the regulation of human RG-specific genes (such as Foxn4) that possibly acquired evolutionary significance.

| S-EPMC6147019 | biostudies-literature

BAF155 methylation at R1064 creates unique chromatin association patterns

Project description:CARM1, a coactivator for various cancer-relevant transcription factors, is overexpressed in breast cancer. To elucidate the functions of CARM1 in tumorigenesis, we knocked out CARM1 from several breast cancer cell lines using Zinc-Finger Nuclease technology, which resulted in drastic phenotypic and biochemical changes. The CARM1 KO cell lines enabled identification of novel CARM1 substrates, notably the SWI/SNF core subunit BAF155. Methylation of BAF155 at R1064 was found to be an independent prognostic biomarker for cancer recurrence and to regulate breast cancer cell migration and metastasis. Further, CARM1-mediated BAF155 methylation affects gene expression by directing methylated BAF155 to unique chromatin regions (e.g., c-Myc pathway genes). Collectively our studies uncover a mechanism by which BAF155 acquires tumorigenic functions via arginine methylation. Examination of methylation of BAF155 (R1064) in breast cancer cells

2014-03-28 | E-GEOD-52964 | biostudies-arrayexpress

Comparison of gene expression in skeletal muscle between Baf155 WT and mutant

Project description:Baf155 is a core subunit of SWI/SNF complex, an ATP dependent chromatin remodeler. To explore the function of Baf155 in skeletal muscle, we deleted the Baf155 in skeletal muscle and compared the gene expression profiling between wild type control and Baf155 deleted mutant mice.

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BAF155 methylation at R1064 creates unique chromatin association patterns

2014-03-28 | GSE52964 | GEO

Baf155 establishes chromatin priming to promote hematopoietic regeneration and function [bulk ATAC]

Project description:Chromatin priming promotes cell type-specific gene expression, lineage differentiation, and development. The mechanism of chromatin priming has not been well understood. Mouse hematopoietic stem and progenitor cells (HSPCs) lacking the Baf155 subunit of the BAF (BRG1/BRM associated factor) chromatin-remodeler produced a significantly reduced number of mature blood cells, leading to a failure of hematopoietic regeneration upon transplantation and 5-FU injury. Baf155 deficient HSPCs, while showing impaired mature blood cell production, generated a higher frequency of myeloid cells with fewer B and CD8+ T cells at homeostasis, supporting a more immune-suppressive tumor microenvironment and enhanced tumor growth. Single-nuclei multi-omic analysis revealed that Baf155 deficient HSPCs failed to establish accessible chromatin and levels of lineage-specific transcripts were considerably lower. Regions that showed a substantial loss in chromatin accessibility were enriched for enhancers and binding motifs for hematopoietic lineage-specific transcription factors. Our study provides a fundamental mechanistic understanding of the role of Baf155 in establishing chromatin priming with functional consequences in regeneration or tumor immunity.

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ENCODE ChIP-chip for BAF155 on Human Hela S3 Cells

Project description:BAF155 ChIP-chip performed on Human Hela S3 Cells for Nimblegen ENCODE arrays which comprise 50mer oligonucleotides spaced every 38bps (overlapping by 12nts). Goal is to identify binding sites for BAF155. Keywords = Transcription Factor Binding, BAF155, ChIP-chip, Human, Genome Tiling Arrays Keywords: ChIP-chip

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Baf155 establishes chromatin priming to promote hematopoietic regeneration and function [single cell multiome - ATAC + GEX]

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BAF155 ChIP-ChIP from K562 Cells using the NimbleGen ENCODE Array [unpublished]

Project description:BAF155 ChIP DNA was isolated from K562 cells and surveyed for binding in the ENCODE regions on NimbleGen ENCODE arrays. Use of this data requires permission from its producers. Keywords: ChIP-chip

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Oligodendroglial hypothesis of autism: the primary role of master regulator gene Baf155 [RNA-Seq]

Project description:Autism spectrum disorders (ASD) are polyetiological neurodevelopmental disorders associated with both genetic and non-genetic risk factors with complex and heterogeneous clinical manifestations. A single susceptibility gene usually fails in triggering an intricate array of autistic symptoms, suggesting a primary mechanism may be required to integrate multiple susceptibility genes in casing the disease. Recent evidence highlights the role of myeline disruption in pathogenesis of ASD. However, neither the mechanisms of impaired myelination nor its contribution to ASD symptomatology are fully characterized. We demonstrate the loss of Baf155, a newly recognized autistic susceptibility gene that encodes a core member of the chromatin remodeling complex, affects oligodendroglial differentiation and myelination. BAF155 targets multiple synapse-related genes in oligodendrocyte precursor cells (OPCs), these genes being responsible for regulating the synaptic communication between OPCs and neurons. Heterogeneous target genes affected by BAF155 deficiency in OPCs across various brain regions leads to significant impairments in myelination which may contribute to the diverse manifestations observed ASD patients. Taken together, our findings reveal a primary mechanism that orchestrates multiple ASD susceptibility genes in instigating the disease.

2025-11-11 | GSE282099 | GEO

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