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Mus musculus

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

PROVIDER: PRJNA383653 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR5460800.fastq.gz	Fastqsanger.gz
	SRR5460801.fastq.gz	Fastqsanger.gz
	SRR5460802.fastq.gz	Fastqsanger.gz
	SRR5460803.fastq.gz	Fastqsanger.gz
	SRR5460804.fastq.gz	Fastqsanger.gz

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Bptf maintains chromatin accessibility and the self-renewal capacity of mammary gland stem cells

Project description:Bptf maintains chromatin accessibility and the self-renewal capacity of mammary gland stem cells

| PRJNA383646 | ENA

Mus musculus

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

| PRJNA383652 | ENA

Mus musculus

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

| PRJNA383654 | ENA

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

2017-06-13 | GSE98003 | GEO

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

2017-06-13 | GSE98002 | GEO

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

2017-06-13 | GSE98001 | GEO

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

miR205 Regulates Mammary Gland Development and Stem Cell Self-renewal through YAP and Wnt signaling

Project description:Mammary gland development is fueled by stem cell self-renewal and differentiation. External cues from the microenvironment coupled with internal cues such as post-transcriptional regulation exerted by miRNAs regulate stem cell behavior and stem cell fate. We have identified a miR205 regulatory network required for mammary gland morphogenesis and stem cell maintenance. In the postnatal mammary gland, miR205 is predominantly expressed in the basal/stem cell enriched population. Conditional deletion of miR205 in mammary epithelial cells severely impaired stem cell self-renewal and mammary repopulating potential both in vitro and in vivo. miR205 null glands displayed significant changes in the basal population, basement membrane and stroma. NKD1 and PP2A-B56, which inhibit the Wnt signaling pathway, and AMOT, which causes YAP cytoplasmic retention and inactivation were identified as miR205 downstream effectors. Collectively these findings reveal an essential role of miR205 in mammary gland development.

2018-12-27 | GSE124364 | GEO

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