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Differential chromatin binding of the lung lineage transcription factor NKX2-1 resolves opposing murine alveolar cell fates in vivo [ATAC-seq]

ABSTRACT: Differential chromatin binding of the lung lineage transcription factor NKX2-1 resolves opposing murine alveolar cell fates in vivo [ATAC-seq]

PROVIDER: PRJNA663783 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12650668_1.fastq.gz	Fastqsanger.gz
	SRR12650668_2.fastq.gz	Fastqsanger.gz
	SRR12650669_1.fastq.gz	Fastqsanger.gz
	SRR12650669_2.fastq.gz	Fastqsanger.gz
	SRR12650670_1.fastq.gz	Fastqsanger.gz

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Similar Datasets

Differential chromatin binding of the lung lineage transcription factor NKX2-1 resolves opposing murine alveolar cell fates in vivo

Project description:Differential chromatin binding of the lung lineage transcription factor NKX2-1 resolves opposing murine alveolar cell fates in vivo

| PRJNA664357 | ENA

Differential chromatin binding of the lung lineage transcription factor NKX2-1 resolves opposing murine alveolar cell fates in vivo [scATAC-Seq]

Project description:Differential chromatin binding of the lung lineage transcription factor NKX2-1 resolves opposing murine alveolar cell fates in vivo [scATAC-Seq]

| PRJNA664332 | ENA

Differential chromatin binding of the lung lineage transcription factor NKX2-1 resolves opposing murine alveolar cell fates in vivo [ChIP-seq]

Project description:Differential chromatin binding of the lung lineage transcription factor NKX2-1 resolves opposing murine alveolar cell fates in vivo [ChIP-seq]

| PRJNA664361 | ENA

Differential chromatin binding of the lung lineage transcription factor NKX2-1 resolves opposing murine alveolar cell fates in vivo [scRNA-Seq]

Project description:Differential chromatin binding of the lung lineage transcription factor NKX2-1 resolves opposing murine alveolar cell fates in vivo [scRNA-Seq]

| PRJNA664459 | ENA

Differential chromatin binding of the lung lineage transcription factor NKX2-1 resolves opposing murine alveolar cell fates in vivo [scRNA-Seq]

Project description:Differential use of identical DNA sequences leads to distinct tissue lineages and then multiple cell types within a lineage, an epigenetic process central to progenitor and stem cell biology. The associated genomic changes, especially in native tissues, remain insufficiently understood, and are hereby addressed in the mouse lung, where the same lineage transcription factor NKX2-1 promotes the diametrically opposed alveolar type 1 (AT1) versus AT2 cell fate. We show that the cell-type-specific function of NKX2-1 is attributed to its differential chromatin binding that is acquired or retained during development in coordination with partner transcriptional factors. Loss of YAP/TAZ redirects NKX2-1 from its AT1-specific to AT2-specific binding sites, leading to transcriptionally exaggerated AT2 cells when deleted in progenitors or AT1-to-AT2 conversion when deleted after fate commitment. Nkx2-1 mutant AT1 and AT2 cells gain distinct accessible sites including those of the opposite fate while adopting the gastrointestinal fate, suggesting an epigenetic plasticity larger than a transcriptional one. Our genomic analysis of single or purified cells, coupled with precision genetics, provides an epigenetic roadmap of alveolar cell fate and potential, and introduces an experimental benchmark for unraveling the in vivo function of lineage transcription factors.

2021-03-08 | GSE158192 | GEO

Differential chromatin binding of the lung lineage transcription factor NKX2-1 resolves opposing murine alveolar cell fates in vivo [ATAC-seq]

2021-03-08 | GSE158024 | GEO

Differential chromatin binding of the lung lineage transcription factor NKX2-1 resolves opposing murine alveolar cell fates in vivo [ChIP-seq]

2021-03-08 | GSE158201 | GEO

Differential chromatin binding of the lung lineage transcription factor NKX2-1 resolves opposing murine alveolar cell fates in vivo [scATAC-Seq]

2021-03-08 | GSE158196 | GEO

Differential chromatin binding of the lung lineage transcription factor NKX2-1 resolves opposing murine alveolar cell fates in vivo.

Project description:Differential transcription of identical DNA sequences leads to distinct tissue lineages and then multiple cell types within a lineage, an epigenetic process central to progenitor and stem cell biology. The associated genome-wide changes, especially in native tissues, remain insufficiently understood, and are hereby addressed in the mouse lung, where the same lineage transcription factor NKX2-1 promotes the diametrically opposed alveolar type 1 (AT1) and AT2 cell fates. Here, we report that the cell-type-specific function of NKX2-1 is attributed to its differential chromatin binding that is acquired or retained during development in coordination with partner transcriptional factors. Loss of YAP/TAZ redirects NKX2-1 from its AT1-specific to AT2-specific binding sites, leading to transcriptionally exaggerated AT2 cells when deleted in progenitors or AT1-to-AT2 conversion when deleted after fate commitment. Nkx2-1 mutant AT1 and AT2 cells gain distinct chromatin accessible sites, including those specific to the opposite fate while adopting a gastrointestinal fate, suggesting an epigenetic plasticity unexpected from transcriptional changes. Our genomic analysis of single or purified cells, coupled with precision genetics, provides an epigenetic basis for alveolar cell fate and potential, and introduces an experimental benchmark for deciphering the in vivo function of lineage transcription factors.

| S-EPMC8096971 | biostudies-literature

PRDM3/16 Regulate Chromatin Accessibility Required for NKX2-1 Mediated Alveolar Epithelial Differentiations and Function [ATAC-seq]

Project description:Differential chromatin accessibility accompanies and mediates transcriptional control of diverse cell fates and their differentiation during embryogenesis. While the critical role of NKX2-1 and its transcritional targets in lung morphogenesis and pulmonary epithelial cell differentiation is increasingly known, mechanisms by which chromatin accessibility alters the epigenetic landscape to regulate NKX2-1 activites required for alveolar epithelial cell differentiation and function are not well understood. Herein, we demonstrate that the paird domain zinc finger transcriptional regulators PRDM3 and PRDM16 regulate chromatin accessibility required for NKX2-1 mediated AT1 and AT2 cell differentiation decisions during lung morphogenesis and for control of the induction of AT@ cell gene expression controlling alveolar function and ventilation at birth. PRDM3 and 16 were required for activation of AT2 cell-associated gene expression, enhancing chromatin accessibility at NKX2-1 transcriptional targets. NKX2-1, PRDM3, and PRDM16 bound together at cis-active DNA elements in AT2 and AT1 cell selective transcriptional target genes, including those critical for perinatal AT2 cell differentitaion, surfactant homeostasis, and innate host defense. Deletion of PRDM3/16 inhibited NKX2-1-dependent gene regulatory networks controlling surfactant lipid and protein production, resulting in respiratory failure at birth. NKX2-1-dependent regulation of alveolar epithelial cell differentiation is mediated by PRDM3/16.

2024-03-01 | GSE250359 | GEO

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