Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

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

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

ORGANISM(S): Mus musculus

PROVIDER: GSE114351 | GEO | 2018/05/11

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

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

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

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

| PRJNA471092 | ENA

H3 acetylation selectively promotes basal progenitor proliferation and neocortex expansion by activating TRNP1 expression

Project description:We performed RNA-Seq and H3K9ac ChIP-Seq from the whole embryonic cortex at E15.5 from BAF155 cKO mice treated either with vehicle or HDAC inhibitor (TSA).

2021-06-05 | GSE176194 | GEO

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.

2023-07-25 | GSE163373 | GEO

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

2005-11-04 | GSE3549 | GEO

BAF155 methylation at R1064 creates unique chromatin association patterns

2014-03-28 | GSE52964 | GEO

Requisite chromatin remodeling for myeloid and erythroid lineage differentiation from erythromyeloid progenitors

Project description:The mammalian SWI/SNF chromatin-remodeling BAF (BRG1/BRM associated factor) complex plays an essential role in developmental and pathological processes. We show that the deletion of Baf155 encoding a subunit of BAF complex in the Tie2(+) lineage (Baf155 CKO) leads to defects in the yolk sac myeloid and definitive erythroid (EryD) lineage differentiation from erythromyeloid progenitors (EMPs) and embryonic lethality. Baf155 knock-down in EMP was sufficient to block myeloid and EryD differentiation. Chromatin of the myeloid gene loci in Baf155 CKO EMPs was largely inaccessible and was enriched mostly by the ETS binding motif. BAF155 interacted with PU.1 and was recruited to the PU.1 in target gene loci together with p300 and KDM6a. Treatment of Baf155 CKO embryos with GSK126, an inhibitor of the H3K27me2/3 methyltransferase EZH2, rescued myeloid lineage gene expression. These studies uncover the indispensable BAF mediated chromatin remodeling of the myeloid gene loci at the EMP stage.

2021-03-08 | GSE159381 | GEO

Requisite chromatin remodeling for myeloid and erythroid lineage differentiation from erythromyeloid progenitors

Project description:The mammalian SWI/SNF chromatin-remodeling BAF (BRG1/BRM-associated factor) complex has an essential role in developmental and pathological processes. We show that deletion of Baf155 encoding a subunit of the BAF complex in the Tie2(+) lineage (Baf155 CKO) leads to defects in yolk sac myeloid and definitive erythroid (EryD) lineage differentiation from erythromyeloid progenitors (EMPs). The chromatin of myeloid gene loci in Baf155 CKO EMPs is mostly inaccessible and enriched mainly by the ETS binding motif. BAF155 interacts with PU.1 and is recruited to PU.1 target gene loci together with p300 and KDM6a. Treatment of Baf155 CKO embryos with GSK126, an H3K27me2/3 methyltransferase EZH2 inhibitor, rescues myeloid lineage gene expression. This study uncovers indispensable BAF-mediated chromatin remodeling of myeloid gene loci at the EMP stage. Future studies exploiting epigenetics in generation and application of EMP derivatives for tissue repair, regeneration, and disease are warranted.

2020-11-17 | GSE144243 | 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.

2024-07-09 | GSE240584 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data