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Release of Notch signaling coordinated by inflammation confers cross-compartment differentiation plasticity during alveolar regeneration.

ABSTRACT: Release of Notch signaling coordinated by inflammation confers cross-compartment differentiation plasticity during alveolar regeneration.

PROVIDER: PRJNA645431 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12195349_1.fastq.gz	Fastqsanger.gz
	SRR12195349_2.fastq.gz	Fastqsanger.gz
	SRR12195350_1.fastq.gz	Fastqsanger.gz
	SRR12195350_2.fastq.gz	Fastqsanger.gz
	SRR12195351_1.fastq.gz	Fastqsanger.gz

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Release of Notch signaling coordinated by inflammation confers cross-compartment differentiation plasticity during alveolar regeneration

Project description:Release of Notch signaling coordinated by inflammation confers cross-compartment differentiation plasticity during alveolar regeneration

| PRJNA643638 | ENA

Release of Notch signaling coordinated by inflammation confers cross-compartment differentiation plasticity during alveolar regeneration

Project description:While the acquisition of cellular plasticity in adult stem cells is essential for rapid restoration after tissue injury, little is known about the underlying molecular mechanisms governing this process. Here, we reveal that Notch signaling is a pivotal determinant conferring cross-compartment differentiation plasticity of airway secretory cells. Temporal Notch inhibition in secretory cells is required for alveolar differentiation upon injury, which is mediated by IL-1β-dependent modulation of Jag1/2 expression in ciliated cells. We also identify Fosl2/Fra2 as an essential transcription factor responsible for the regeneration of secretory cell-derived alveolar type 2 (sAT2) cells retaining distinct genetic/epigenetic features. We furthermore reveal that KDR/FLK-1+ human secretory cells display a conserved capacity to generate AT2 cells via Notch inhibition. Our results demonstrate that Notch signaling acts as a functional rheostat for fate decision of secretory cells during injury repair, proposing a new potential therapeutic target for human lung alveolar regeneration.

2021-09-08 | GSE153677 | GEO

Release of Notch signaling coordinated by inflammation confers cross-compartment differentiation plasticity during alveolar regeneration.

Project description:While the acquisition of cellular plasticity in adult stem cells is essential for rapid restoration after tissue injury, little is known about the underlying molecular mechanisms governing this process. Here, we reveal that Notch signaling is a pivotal determinant conferring cross-compartment differentiation plasticity of airway secretory cells. Temporal Notch inhibition in secretory cells is required for alveolar differentiation upon injury, which is mediated by IL-1β-dependent modulation of Jag1/2 expression in ciliated cells. We also identify Fosl2/Fra2 as an essential transcription factor responsible for the regeneration of secretory cell-derived alveolar type 2 (sAT2) cells retaining distinct genetic/epigenetic signatures. We furthermore reveal that KDR/FLK-1+ human secretory cells display a conserved capacity to generate AT2 cells via Notch inhibition. Our results demonstrate that Notch signaling acts as a functional rheostat for fate decision of secretory cells during injury repair, proposing a new potential therapeutic target for human lung alveolar regeneration.

2021-09-08 | GSE154218 | GEO

Effects of acute Notch activation on the mammary epithelial compartment in vivo

Project description:Notch signaling is widely implicated in mouse mammary gland development and tumorigenesis. To investigate the effects of acute activation of Notch signaling in the mammary epithelial compartment, we generated bi-transgenic MMTV-rtTA; TetO-NICD1 (MTB/TICNX) mice that conditionally express a constitutively active NOTCH1 intracellular domain (NICD1) construct in the mammary epithelium upon doxycycline administration.

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Compartment-specific and HuR-coordinated regulation of intronic polyadenylation isoforms by doxorubicin

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Notch induces transcription by stimulating release of paused RNA Pol II without increasing chromatin accessibility [ATAC-seq]

Project description:Notch proteins undergo ligand-induced proteolysis to release a nuclear effector that influences a wide range of cell fate decisions by regulating gene activity. However, despite years of study, how Notch induces the transcription of its target genes remains unclear. Here, we comprehensively examined the response to human Notch1 across a time course of activation, using genomic assays of nascent RNA and chromatin accessibility. These data revealed that Notch induces target gene transcription primarily by releasing paused RNA polymerase II (RNAPII), in contrast to prevailing models suggesting that Notch acts by promoting chromatin accessibility. Indeed, we found that open chromatin is established at Notch-responsive regulatory elements prior to Notch signaling, through SWI/SNF-mediated remodeling. Notch activation, however, elicited no further chromatin opening at these loci. Together, these studies reveal that the nuclear response to Notch signaling is dictated by the pre-existing chromatin state and RNAPII distribution at the time of signal activation.

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Notch induces transcription by stimulating release of paused RNA Pol II without increasing chromatin accessibility [ChIP-seq]

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Notch induces transcription by stimulating release of paused RNA Pol II without increasing chromatin accessibility [TT-seq]

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