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

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus

PROVIDER: GSE108441 | GEO | 2018/01/25

REPOSITORIES: GEO

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The Chromatin Remodeler BPTF Activates a Stemness Gene-Expression Program Essential for the Maintenance of Adult Hematopoietic Stem Cells.

Project description:Self-renewal and differentiation of adult stem cells are tightly regulated partly through configuration of chromatin structure by chromatin remodelers. Using knockout mice, we here demonstrate that bromodomain PHD finger transcription factor (BPTF), a component of the nucleosome remodeling factor (NURF) chromatin-remodeling complex, is essential for maintaining the population size of hematopoietic stem/progenitor cells (HSPCs), including long-term hematopoietic stem cells (HSCs). Bptf-deficient HSCs are defective in reconstituted hematopoiesis, and hematopoietic-specific knockout of Bptf caused profound defects including bone marrow failure and anemia. Genome-wide transcriptome profiling revealed that BPTF loss caused downregulation of HSC-specific gene-expression programs, which contain several master transcription factors (Meis1, Pbx1, Mn1, and Lmo2) required for HSC maintenance and self-renewal. Furthermore, we show that BPTF potentiates the chromatin accessibility of key HSC "stemness" genes. These results demonstrate an essential requirement of the chromatin remodeler BPTF and NURF for activation of "stemness" gene-expression programs and proper function of adult HSCs.

| S-EPMC5918338 | biostudies-literature

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.

2018-01-25 | GSE108440 | GEO

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

2018-01-25 | GSE108439 | GEO

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

2018-01-25 | GSE108438 | GEO

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

Project description:The chromatin remodeler Bptf activates a stemness gene-expression program essential for the maintenance of adult hematopoietic stem cells

| PRJNA427284 | ENA

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

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

| PRJNA427309 | ENA

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

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

| PRJNA427308 | ENA

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

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

| PRJNA427310 | ENA

Chromatin analysis of adult pluripotent stem cells reveals a unique stemness maintenance strategy.

Project description:Many highly regenerative organisms maintain adult pluripotent stem cells throughout their life, but how the long-term maintenance of pluripotency is accomplished is unclear. To decipher the regulatory logic of adult pluripotent stem cells, we analyzed the chromatin organization of stem cell genes in the planarian Schmidtea mediterranea. We identify a special chromatin state of stem cell genes, which is distinct from that of tissue-specific genes and resembles constitutive genes. Where tissue-specific promoters have detectable transcription factor binding sites, the promoters of stem cell-specific genes instead have sequence features that broadly decrease nucleosome binding affinity. This genic organization makes pluripotency-related gene expression the default state in these cells, which is maintained by the activity of chromatin remodelers ISWI and SNF2 in the stem cells.

| S-EPMC10558129 | biostudies-literature

Haploinsufficiency of the Chromatin Remodeler BPTF Causes Syndromic Developmental and Speech Delay, Postnatal Microcephaly, and Dysmorphic Features.

Project description:Bromodomain PHD finger transcription factor (BPTF) is the largest subunit of nucleosome remodeling factor (NURF), a member of the ISWI chromatin-remodeling complex. However, the clinical consequences of disruption of this complex remain largely uncharacterized. BPTF is required for anterior-posterior axis formation of the mouse embryo and was shown to promote posterior neuroectodermal fate by enhancing Smad2-activated wnt8 expression in zebrafish. Here, we report eight loss-of-function and two missense variants (eight de novo and two of unknown origin) in BPTF on 17q24.2. The BPTF variants were found in unrelated individuals aged between 2.1 and 13 years, who manifest variable degrees of developmental delay/intellectual disability (10/10), speech delay (10/10), postnatal microcephaly (7/9), and dysmorphic features (9/10). Using CRISPR-Cas9 genome editing of bptf in zebrafish to induce a loss of gene function, we observed a significant reduction in head size of F0 mutants compared to control larvae. Terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) and phospho-histone H3 (PH3) staining to assess apoptosis and cell proliferation, respectively, showed a significant increase in cell death in F0 mutants compared to controls. Additionally, we observed a substantial increase of the ceratohyal angle of the craniofacial skeleton in bptf F0 mutants, indicating abnormal craniofacial patterning. Taken together, our data demonstrate the pathogenic role of BPTF haploinsufficiency in syndromic neurodevelopmental anomalies and extend the clinical spectrum of human disorders caused by ablation of chromatin remodeling complexes.

| S-EPMC5630163 | biostudies-literature

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