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

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

PROVIDER: PRJNA383646 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR5460780.fastq.gz	Fastqsanger.gz
	SRR5460790.fastq.gz	Fastqsanger.gz
	SRR5460800.fastq.gz	Fastqsanger.gz
	SRR5460781.fastq.gz	Fastqsanger.gz
	SRR5460791.fastq.gz	Fastqsanger.gz

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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.

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

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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.

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 mammary epithelial cells (MECs). 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 or chemical inhibition, suggests a role for BPTF in maintaining the open chromatin landscape at enhancers regions in 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

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Project description:Understanding the mechanism by which embryonic stem (ES) cells self-renew is critical for the realization of their therapeutic potential. Previously it had been shown that in combination with LIF, Id proteins were sufficient to maintain mouse ES cells in a self-renewing state. Here we investigate the requirement for Id1 in maintaing ES cell self-renewal and blocking differentiation. We find that Id1-/- ES cells have a propensity to differentiate and a decreased capacity to self-renew. Chronic or acute loss of Id1 leads to a down-regulation of Nanog, a critical regulator of self-renewal. In addition, in the absence of Id1, ES cells express elevated levels of Brachyury, a marker of mesendoderm differentiation. We find that loss of both Nanog and Id1 is required for the up-regulation of Brachyury, and Id1 maintains Nanog expression by blocking the expression of Zeb1, a repressor of Nanog transcription. These results identify Id1 as an important factor in the maintenance of ES cell self-renewal and suggest a plausible mechanism for its control of lineage commitment. Wild type and Id1-/- ES cells were grown on gelatin under normal self-renewing conditions (in the presence of serum and LIF).

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