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CEBPA restricts alveolar type 2 cell plasticity during development and injury-repair [scATAC-seq]

ABSTRACT: CEBPA restricts alveolar type 2 cell plasticity during development and injury-repair [scATAC-seq]

PROVIDER: PRJNA1100986 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR28735385.fastq.gz	Fastqsanger.gz
	SRR28735385_1.fastq.gz	Fastqsanger.gz
	SRR28735385_2.fastq.gz	Fastqsanger.gz
	SRR28735386.fastq.gz	Fastqsanger.gz
	SRR28735386_1.fastq.gz	Fastqsanger.gz

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CEBPA restricts alveolar type 2 cell plasticity during development and injury-repair [scATAC-seq]

Project description:Cell plasticity theoretically extends to all possible cell types, but naturally decreases as cells differentiate, whereas injury-repair re-engages the developmental plasticity. Here we show that the lung alveolar type 2 (AT2)-specific transcription factor (TF), CEBPA, restricts AT2 cell plasticity in the mouse lung. AT2 cells undergo transcriptional and epigenetic maturation postnatally. Without CEBPA, both neonatal and mature AT2 cells reduce the AT2 program, but only the former reactivate the SOX9 progenitor program. Sendai virus infection bestows mature AT2 cells with neonatal plasticity where Cebpa mutant, but not wild type, AT2 cells express SOX9, as well as more readily proliferate and form KRT8/CLDN4+ transitional cells. CEBPA promotes the AT2 program by recruiting the lung lineage TF NKX2-1. The temporal change in CEBPA-dependent plasticity reflects AT2 cell developmental history. The ontogeny of AT2 cell plasticity and its transcriptional and epigenetic mechanisms have implications in lung regeneration and cancer.

2024-04-16 | GSE264098 | GEO

CEBPA restricts alveolar type 2 cell plasticity during development and injury-repair [1]

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CEBPA restricts alveolar type 2 cell plasticity during development and injury-repair [ChIP-seq]

2024-04-19 | GSE247271 | GEO

CEBPA restricts alveolar type 2 cell plasticity during development and injury-repair

Project description:CEBPA restricts alveolar type 2 cell plasticity during development and injury-repair

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CEBPA restricts alveolar type 2 cell plasticity during development and injury-repair [1]

Project description:CEBPA restricts alveolar type 2 cell plasticity during development and injury-repair [1]

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CEBPA restricts alveolar type 2 cell plasticity during development and injury-repair [ChIP-seq]

Project description:CEBPA restricts alveolar type 2 cell plasticity during development and injury-repair [ChIP-seq]

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CEBPA restricts alveolar type 2 cell plasticity during development and injury-repair.

| S-EPMC10760240 | biostudies-literature

CEBPA restricts alveolar type 2 cell plasticity during development and injury-repair

Project description:This SuperSeries is composed of the SubSeries listed below.

2024-04-17 | GSE247272 | GEO

Maternal IL-10 restricts fetal emergency myelopoiesis [scATAC-seq]

Project description:Maternal IL-10 restricts fetal emergency myelopoiesis [scATAC-seq]

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The p30 isoform of CEBPA uncovers a silent enhancer to drive the expression of the tumor promoting factor CD73 in CEBPA mutant AML

Project description:The key myeloid transcription factor (TF) CEBPA is frequently mutated in acute myeloid leukemia (AML), but the molecular ramifications of this leukemic driver mutation remain elusive. To investigate CEBPA mutant AML, we compared gene expression changes in human CEBPA mutant AML and in the corresponding CebpaLp30 mouse model, and identified a conserved cross-species transcriptional program. ChIP-seq revealed aberrantly activated enhancers, exclusively occupied by the leukemia-associated CEBPA-p30 isoform. One leukemic-enhancer upstream of Nt5e, encoding CD73, was physically and functionally linked to this conserved AML gene, and could be activated by CEBPA. Targeting of CD73-adenosine signaling increased AML survival in transplanted mice. Our data indicate a first-in-class link between a TF cancer driver mutation and a druggable, direct transcriptional target.

2019-08-08 | PXD011359 | Pride

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