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Eda-activated RelB recruits an SWI/SNF (BAF) chromatin-remodeling complex and initiates gene transcription in skin appendage formation

ABSTRACT: Skin-specific Eda signaling promotes skin appendage development through NF-kB mediated gene transcription. We find that Eda triggers the formation of a novel SWI/SNF complex in which RelB is recruited through a linker protein, Tfg, to interact with the BAF45d component in SWI/SNF (BAF) chromatin remodeling complex. BAF component BAF250a is particularly enriched in skin appendages, and epidermal knockout (cKO) of BAF250a impairs skin appendage development, resulting in phenotypes similar to those of Eda-deficient mouse models. We further reveal that Eda signaling is predominantly mediated by the p50/RelB subclass of NF-kB in both human keratinocytes and mouse skin. Consistent with the phenotype of BAF250a cKO mice, downregulation of RelB, Tfg, or BAF45d arrests the growth of Meibomian gland germs in organ cultures. Transcription profiling consistently identifies several target genes regulated by Eda, RelB and SWI/SNF. In particular, we show that both RelB and SWI/SNF are indispensable for transcription of Eda target Ltb. Chromatin remodeling SWI/SNF recruited to specific gene loci by Eda-activated RelB thus provides a mediation model between an initiation signal and gene activation in organogenesis.

ORGANISM(S): Homo sapiens

PROVIDER: GSE97783 | GEO | 2018/07/24

REPOSITORIES: GEO

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Homo sapiens

Project description:Eda-activated RelB recruits an SWI/SNF (BAF) chromatin-remodeling complex and initiates gene transcription in skin appendage formation

| PRJNA382853 | ENA

ARID-DNA interactions are essential for SWI/SNF function

Project description:Every known SWI/SNF chromatin-remodeling complex incorporates an ARID DNA binding domain-containing subunit. Despite being a ubiquitous component of these complexes, physiological roles for this domain remain undefined. We screened an N-ethyl-N-nitrosurea (ENU) mutagenized library for ARID domain point mutations and generated an Arid1a/Baf250a hypomorphic allele. The mutant ARID1a (V1068G) protein is stably expressed at wild-type levels, and it is capable of assembling into a SWI/SNF complex with in vitro mononucleosome disruption activity. However, its capacity to bind DNA is lost. Consistent with defective DNA binding, mutant protein occupancy at known SWI/SNF target genes is decreased. Loss of DNA binding is associated with concurrent changes in SWI/SNF target gene expression. Mutant embryos manifest heart defects, fail to establish proper yolk sac vasculature, and exhibit hemorrhaging. As a result of these phenotypes, mutant embryos fail to establish proper circulation, culminating in ischemic arrest in utero between days 9.5 and 11.5. These data support a role for ARID1a-containing, BAF-A complexes in heart and extraembryonic vascular development, and indicate the ARID domain of ARID1a is essential in this regard. Hence, intrinsic ARID subunit-DNA interactions are required for normal SWI/SNF function in vivo. Four-condition experiment, wild-type vs Baf250a/Arid1a^V1068G/V1068G yolk sacs isolated at E8.5 and E9.5. Biological replicates: 3 per condition.

2012-01-15 | E-GEOD-32116 | biostudies-arrayexpress

Differential requirements for the BAF and ncBAF subfamilies of the mammalian SWI/SNF chromatin remodeling enzymes during skeletal muscle differentiation.

Project description:Subunit proteins BAF250a and Brd9 are specific to mammalian SWI/SNF subfamilies BAF and ncBAF respectively. We have performed RNA-seq analysis for C2C12 myoblasts stably knocked down for each subunits using specific shRNA constructs. C2C12 cells stably transfected with non-targeting scrambled shRNA construct were used as controls.

2023-07-10 | GSE196281 | GEO

The study of dpf2 in mouse ES cells

Project description:Brg-or Brm-associated factor (BAF) complexes, is a 12 subunit complex which contains an ATPase subunit, Brg or Brm, that uses energy derived from ATP hydrolysis to disrupt histone:DNA contacts to catalyze transcriptional events such as promoting gene expression or repression. Genetic studies in mice demonstrated that BAF complexes are essential for early embryonic development and pluripotency. ES cells express distinctive compleses, termed esBAF complexes by the presence of BAF155, Brg, BAF60a. Purification of Brg and Brm-associated proteins reveals a new family of four stoichiometric subunits of mSWI/SNF or BAF complexes which was termed BAF45a, b, c, and d. The progenitors to both neurons and glia are maintained in a proliferative state by a specified SWI/SNF-like npBAF complex that contains both BAF45a and BAF53a. The transition from proliferative to neurogenic divisions requires the exchange of these subunites for the homologous BAF45b or BAF45c and BAF53b proteins. The function of BAF45d remwains unclear so far.At present, we found that the knockout of dpf2 in ES cells impared the differention of ES cells. We will identify the target genes of dpf2 by Chip-seq so that we could study how dpf2 affect the differentiation of ES cells into germ layers.Protocol: DNA was prepared from ES cells by standard ChIP method. This data is part of a pre-publication release. For information on the proper use of pre-publication data shared by the Wellcome Trust Sanger Institute (including details of any publication moratoria), please see http://www.sanger.ac.uk/datasharing/

2013-09-30 | E-ERAD-24 | biostudies-arrayexpress

BCL7A-containing SWI/SNF/BAF complexes modulate mitochondrial bioenergetics during neural progenitor differentiation.

Project description:Mammalian SWI/SNF/BAF chromatin remodeling complexes influence cell lineage determination. While the contribution of mammalian SWI/SNF/BAF complexes in neural progenitor cell (NPC) proliferation and differentiation has been reported, little is known about the transcriptional profiles that determine neurogenesis or gliogenesis. Here we report that BCL7A is a modulator of the SWI/SNF/BAF complex and stimulates the genome-wide occupancy of the ATPase BRG1. We demonstrate that BCL7A is dispensable for SWI/SNF/BAF complex integrity, whereas it is essential to regulate Notch/Wnt pathway and mitochondrial bioenergetics in differentiating NPCs. Together, our findings uncover the unique mechanistic contribution of BCL7A-containing SWI/SNF/BAF complex in mitochondria-driven NPC commitment, thereby providing a better understanding of the cell-intrinsic transcriptional processes that connect metabolism, neuronal morphogenesis and cognitive flexibility.

2022-10-15 | GSE210759 | GEO

BCL7A-containing SWI/SNF/BAF complexes modulate mitochondrial bioenergetics during neural progenitor differentiation.

2022-10-15 | GSE210757 | GEO

BCL7A-containing SWI/SNF/BAF complexes modulate mitochondrial bioenergetics during neural progenitor differentiation.

2022-10-15 | GSE210756 | GEO

Different SWI/SNF complexes coordinately promote R-loop- and RAD52- dependent transcription-coupled homologous recombination

Project description:The SWI/SNF family of ATP-dependent chromatin remodeling complexes are implicated in multiple DNA damage response mechanisms and frequently mutated in cancer. The BAF and PBAF complexes are two major types of SWI/SNF complexes that are functionally distinguished by their exclusive subunits. Accumulating evidence suggests that double-strand breaks (DSBs) in transcriptionally active DNA are preferentially repaired by a dedicated homologous recombination pathway. We show that different BAF and PBAF subunits promote homologous recombination and are rapidly recruited to DSBs in a transcription-dependent manner. The PBAF complex promotes RNA polymerase II eviction near DNA damage to rapidly initiate transcriptional silencing, while the BAF complex helps to maintain this transcriptional silencing. Furthermore, ARID1A-containing BAF complexes promote RNaseH1 and RAD52 recruitment to facilitate R-loop resolution and DNA repair. Our results highlight how multiple SWI/SNF complexes perform different functions to enable DNA repair in the context of actively transcribed genes.

2023-07-31 | PXD035140 | Pride

BAF250a regulates nucleosome occupancy and histone modification in priming embryonic stem cell differentiation

Project description:BAF complex is one major group of chromatin remodeling factors in mammals. However, how BAF regulated nucleosomes and other histone modifications is not clear. Here we delete BAF250a, a major component in esBAF to study the nucleosome and histone changes in ESCs. We find that deletion of BAF250a leads to nucleosome occupancy increase in TSS regions and non-pioneer transcription factor binding sites. BAF250a deletion also cause overall decrease of H3K27me3 modification. Collectively, these results reveals how BAF complex coordinates nucleosome, histone modification to control ESC function. Sample 1-4: Nucleosome profiles in WT and BAF250a KO ESCs. Sample 5-10: profiling of H3K4me3 and H3K27me3 in WT and BAF250 KO ESCs.

2015-08-03 | E-GEOD-59082 | biostudies-arrayexpress

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

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