A non-canonical BRD9-containing BAF chromatin remodeling complex regulates naive pluripotency in mouse embryonic stem cells

Gatchalian, Jovylyn; Malik, Sunita; Ho, Josephine; Lee, Dong-Sung; Kelso, Timothy W. R.; Shokhirev, Maxim N.; Dixon, Jesse R.; Hargreaves, Diana C.

doi:10.1038/s41467-018-07528-9

Cited by 170 publications

(251 citation statements)

References 61 publications

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“…When compared with canonical BAF, GBAF localizes to both distinct and shared genomic regions. GBAF is more enriched at sites marked with H3K4me3, and it also uniquely localizes to topologically associating domain (TAD) boundaries (Gatchalian et al, 2018;Michel et al, 2018). In BAF-perturbed synovial sarcoma and malignant rhabdoid tumors, GBAF is necessary to maintain gene expression at retained promoter-proximal and CTCF sites.…”

Section: Unique Characteristics Of the Gbaf Complexmentioning

confidence: 99%

Unwinding chromatin at the right places: how BAF is targeted to specific genomic locations during development

Lloyd

Bao

2019

Development

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The BAF (SWI/SNF) chromatin remodeling complex plays a crucial role in modulating spatiotemporal gene expression during mammalian development. Although its remodeling activity was characterized in vitro decades ago, the complex actions of BAF in vivo have only recently begun to be unraveled. In living cells, BAF only binds to and remodels a subset of genomic locations. This selectivity of BAF genomic targeting is crucial for cell-type specification and for mediating precise responses to environmental signals. Here, we provide an overview of the distinct molecular mechanisms modulating BAF chromatin binding, including its combinatory assemblies, DNA/histone modification-binding modules and post-translational modifications, as well as its interactions with proteins, RNA and lipids. This Review aims to serve as a primer for future studies to decode the actions of BAF in developmental processes.

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Section: Unique Characteristics Of the Gbaf Complexmentioning

confidence: 99%

Unwinding chromatin at the right places: how BAF is targeted to specific genomic locations during development

Lloyd

Bao

2019

Development

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“…Additionally, OTX015 (MK‐8628), a novel BRD2/3/4 inhibitor, showed a synergistic to additive activity when administered concomitant to temozolomide or everolimus in glioma models . Targeting BRDs‐ and E2F1‐dependent transcriptional program maintains the malignancy of glioma, and BRD9 interacts with BRD4 to regulate naive pluripotency in mouse embryonic stem cells . Since the cancer stem cells (CSCs) have similar characteristics to normal embryonic stem cells, that is, self‐renewal ability, we speculate that BRD4 holds critical roles in glioma cell stemness.…”

Section: Introductionmentioning

confidence: 97%

BRD4 promotes glioma cell stemness via enhancing miR‐142‐5p‐mediated activation of Wnt/β‐catenin signaling

Wang

et al. 2019

Environmental Toxicology

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The bromodomain protein BRD4 exerts carcinogenic effects in many cancers. However, its roles in glioma occurrence are still confused. Here, it is found that BRD4 expression is increased in glioma tissues and negatively correlated with the overall survival of glioma patients. We construct cellular experiments indicating that BRD4 promotes glioma cell stemness by analyzing ALDH1 activity, master stemness regulator expression, and sphere formation ability. Mechanistically, BRD4 knockdown triggers a switch of miR-142-5p promoter methylation, which targets Wnt3a and thus further inactivates Wnt/β-catenin signaling. Importantly, inhibition of miR-142-5p or reactivation of Wnt/β-catenin signaling rescues the inhibition of BRD4 knockdown on glioma cell stemness. As a result, these results not only indicate an unforeseen connection between BRD4, miR-142-5p, and Wnt/β-catenin signaling, but also reveal a promising epigenetic-based therapeutic strategy that might be explored for glioma patients. K E Y W O R D SBRD4, glioma, miR-142-5p, Stemness, Wnt/β-catenin

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“…The enzymatic activity of the mSWI/SNF complexes are driven by the ATPase Brahma-related gene 1 (Brg1) or Brahma (Brm) [2,[7][8][9]. There are many associated subunits that combine in an ordered manner [10] to form different subfamilies of complexes that contain both common and unique subunits [10][11][12][13][14]. The great diversity of enzyme complex assemblies is thought to enable cell-and developmental stage-specific functions [14,15].…”

Section: Introductionmentioning

confidence: 99%

CK2-Dependent Phosphorylation of the Brg1 Chromatin Remodeling Enzyme Occurs during Mitosis

Padilla‐Benavides

Haokip

Yoon

et al. 2020

IJMS

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Brg1 (Brahma-related gene 1) is one of two mutually exclusive ATPases that can act as the catalytic subunit of mammalian SWI/SNF (mSWI/SfigureNF) chromatin remodeling enzymes that facilitate utilization of the DNA in eukaryotic cells. Brg1 is a phospho-protein, and its activity is regulated by specific kinases and phosphatases. Previously, we showed that Brg1 interacts with and is phosphorylated by casein kinase 2 (CK2) in a manner that regulates myoblast proliferation. Here, we use biochemical and cell and molecular biology approaches to demonstrate that the Brg1-CK2 interaction occurred during mitosis in embryonic mouse somites and in primary myoblasts derived from satellite cells isolated from mouse skeletal muscle tissue. The interaction of CK2 with Brg1 and the incorporation of a number of other subunits into the mSWI/SNF enzyme complex were independent of CK2 enzymatic activity. CK2-mediated hyperphosphorylation of Brg1 was observed in mitotic cells derived from multiple cell types and organisms, suggesting functional conservation across tissues and species. The mitotically hyperphosphorylated form of Brg1 was localized with soluble chromatin, demonstrating that CK2-mediated phosphorylation of Brg1 is associated with specific partitioning of Brg1 within subcellular compartments. Thus, CK2 acts as a mitotic kinase that regulates Brg1 phosphorylation and subcellular localization.

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A non-canonical BRD9-containing BAF chromatin remodeling complex regulates naive pluripotency in mouse embryonic stem cells

Cited by 170 publications

References 61 publications

Unwinding chromatin at the right places: how BAF is targeted to specific genomic locations during development

Unwinding chromatin at the right places: how BAF is targeted to specific genomic locations during development

BRD4 promotes glioma cell stemness via enhancing miR‐142‐5p‐mediated activation of Wnt/β‐catenin signaling

CK2-Dependent Phosphorylation of the Brg1 Chromatin Remodeling Enzyme Occurs during Mitosis

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