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Nucleosome occupancy measurments in Bptf knockout ESC, MEF and DP thymocytes.

ABSTRACT: NURF is a remodleing complex expressed in many cell types. Knockout of Bptf, the unique and essental subunit of NURF, results in altered nucleosome occupancy across the genome. To measure changes in nucleosome occupancy we hybridized nucleosomal DNA overdigested with MNase to 10 bp tiling arrays covering 3.3 Mbp of the mouse genome.

ORGANISM(S): Mus musculus

PROVIDER: GSE47416 | GEO | 2014/11/06

SECONDARY ACCESSION(S): PRJNA205525

REPOSITORIES: GEO

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Genome-wide measurement of gene expression changes with Bptf knockout in mouse embryonic fibroblasts

Project description:Gene expression frequently requires the action of chromatin remodeling complexes and it is assumed that these complexes have common gene targets across cell-types. Contrary to this belief, we show that Bptf, an essential and unique subunit of the Nucleosome Remodeling Factor (NURF), largely regulates cell-type-restricted gene expression across diverse cell-types. Unexpectedly, cell-type-restricted gene expression is accomplished through both physical and functional interactions between NURF and the ubiquitous multivalent factor Ctcf. We go on to show in these cell types, that Bptf influences the regulatory activity of Ctcf binding sites in a cell type-restricted manner. Detailed studies of Ctcf binding sites in embryonic stem cells (ESC) show that Bptf prevents Klf4 binding upstream of H2-K1, and facilitates RNA polymerase elongation through Ccnd1, to regulate genes important for embryonic development. In total, these studies provide mechanisms by which prominent chromatin remodeling complexes can maintain cell-type-restricted gene expression through ubiquitous factors like Ctcf.

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BPTF is required for c-MYC-induced remodelling of target chromatin and transcriptional activation [RNA-Seq]

Project description:The c-MYC oncogene is a key transcription factor deregulated in most human tumors. Histone marks associated with transcriptionally active genes in euchromatic islands define the set of high-affinity c-MYC targets. The mechanisms involved in their recognition by c-MYC are not known but likely involve chromatin-remodelling and chromatin-modifying complexes. Here, we show that c-MYC interacts with BPTF, a core subunit of the NURF complex that binds active chromatin. BPTF is required for the activation of the full c-MYC transcriptional programme in fibroblasts. BPTF knockdown leads to a decrease in c-MYC recruitment to DNA and to changes in chromatin accessibility. Using BPTF-null MEFs we show that BPTF is necessary for c-MYC-driven proliferation, G1-S progression, and replication stress, but not for c-MYC-driven apoptosis. Consistently, BPTF is required for the proliferation of cells driven by c-MYC, such as Burkitt lymphoma, and its expression in human cancer lines correlates with the activation of c-MYC gene signatures. Our findings point to the c-MYC-BPTF axis as a potential therapeutic target in cancer. To assess whether BPTF is required for the transcriptional activity of c-MYC, human foreskin fibroblasts (HFF) were stably transduced with the chimeric MYC-ER cDNA (HFF MYC-ER) and infected with lentiviruses coding for either control (shNt) or BPTF-targeting shRNAs. Cells were serum-starved for 2 days to achieve quiescence and then treated with 4-hydroxytamoxifen (4-OHT)

2016-01-19 | E-GEOD-65545 | biostudies-arrayexpress

BPTF is required for c-MYC-induced remodelling of target chromatin and transcriptional activation [ChIP-Seq]

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The chromatin remodeler Bptf activates a stemness gene-expression program essential for the maintenance of adult hematopoietic stem cells [ChIP-Seq]

Project description:Bptf, a component of NURF chromatin-remodeling complex, is essential for maintaining the pool size and function of hematopoietic stem cells (HSCs). Genome-wide transcriptome profiling revealed that Bptf loss caused down-regulation of HSC-specific gene-expression programs, which included master transcription factors (such as Meis1, Pbx1, and Lmo2) known to be required for HSC maintenance and self-renewal. Bptf directly bound to the promoter of ‘stemness’ TF genes, potentiating their transcription and DNA accessibility.

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The chromatin remodeler Bptf activates a stemness gene-expression program essential for the maintenance of adult hematopoietic stem cells [ATAC-Seq]

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The chromatin remodeler Bptf activates a stemness gene-expression program essential for the maintenance of adult hematopoietic stem cells [RNA-Seq]

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Bptf maintains chromatin accessibility and the self-renewal capacity of mammary gland stem cells [ChIP-Seq]

Project description:Chromatin remodeling is a key requirement for transcriptional control of cellular differentiation. However, the factors that alter chromatin architecture in mammary stem cells (MaSCs) are poorly understood. Here we show that Bptf, the largest subunit of the NURF chromatin remodeling complex, is essential for MaSC self-renewal and differentiation of epithelial cells in the mammary gland. Bptf depletion arrests cells at a previously undefined stage of epithelial differentiation that is associated with an incapacity to achieve the luminal cell fate. Moreover, genome-wide analysis of DNA accessibility following genetic and chemical inhibition of Bptf, suggests a role for this factor in maintaining the open chromatin landscape of cis-regulatory elements in mammary epithelial cells (MECs). Collectively, our study implicates Bptf in maintaining the unique epigenetic state of MaSCs.

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Bptf maintains chromatin accessibility and the self-renewal capacity of mammary gland stem cells [ATAC-Seq]

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Bptf maintains chromatin accessibility and the self-renewal capacity of mammary gland stem cells [RNA-Seq]

2017-06-13 | GSE98003 | GEO

BPTF is essential for murine neocortical development

Project description:Chromatin remodeling complexes modulate DNA accessibility permitting neuronal progenitor cells to proliferate and differentiate to form the mammalian neocortex. In the case of BPTF, the major subunit of a chromatin remodelling complex called NURF, mutations leading to its haploinsufficiency have been linked to cause a recently annotated human neurodevelopmental disorder called NEDDFL (Neurodevelopmental disorder with dysmorphic facies and distal limb anomalies). Patients with this syndrome are mainly characterized with microcephaly and intellectual disability. We conditionally knockout (cKO) the Bptf gene during neocortical neurogenesis to analyze its role during embryonic and postnatal brain development. The Bptf cKO animals reveal significant forebrain hypoplasia. During cortical neurogenesis, the cKOs show a reduction in intermediate neuronal progenitor (INP) cells, an increase in apoptosis as well as a prolonged cell cycle of proliferating progenitors. Similarly, the cKOs have decreased proportions of pyramidal neurons expressing Ctip2 and Foxp1. Lastly, our RNA-seq analysis delineates gene pathways deregulated by Bptf’s removal, which are involved in neurogenesis and neuronal differentiation. Our results indicate that Bptf is critical for murine telencephalon neurogenesis. The hypoplasia demonstrated in the mouse model can resemble the microcephaly displayed by the human NEDFFL patients, highlighting the relevance of chromatin remodelling complexes during intricate neural developmental processes.

2022-03-31 | GSE154700 | GEO

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