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Dynamic Hippo pathway activity underlies mesenchymal differentiation during lung alveolar morphogenesis

ABSTRACT: Dynamic Hippo pathway activity underlies mesenchymal differentiation during lung alveolar morphogenesis

PROVIDER: PRJNA1073446 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR27872763_1.fastq.gz	Fastqsanger.gz
	SRR27872763_2.fastq.gz	Fastqsanger.gz
	SRR27872764_1.fastq.gz	Fastqsanger.gz
	SRR27872764_2.fastq.gz	Fastqsanger.gz
	SRR27872765_1.fastq.gz	Fastqsanger.gz

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Dynamic Hippo pathway activity underlies mesenchymal differentiation during lung alveolar morphogenesis [bulk RNA-seq]

Project description:Dynamic Hippo pathway activity underlies mesenchymal differentiation during lung alveolar morphogenesis [bulk RNA-seq]

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Dynamic Hippo pathway activity underlies mesenchymal differentiation during lung alveolar morphogenesis

Project description:Alveologenesis, the final stage in lung development, substantially remodels the distal lung, expanding the alveolar surface area for efficient gas exchange. Secondary crest myofibroblasts (SCMF) exist transiently in the neonatal distal lung and are critical for alveologenesis. However, the pathways that regulate SCMF function, proliferation, and temporal identity remain poorly understood. To address this, we purified SCMFs from reporter mice, performed bulk RNA-sequencing, and found dynamic changes in Hippo-signaling components during alveologenesis. We deleted Hippo effectors, Yap/Taz, from Acta2-expressing SCMFs at the onset of alveologenesis, causing a significant arrest in alveolar development. Using scRNA-seq, we identified a distinct cluster of cells in mutant lungs with altered expression of marker genes associated with proximal mesenchymal cell types, airway smooth muscle (ASM), and alveolar duct myofibroblasts (DMF). Using lineage tracing, we show that neonatal Acta2-expressing SCMFs give rise to adult DMFs and that Yap/Taz mutants have an increase of persisting DMF-like cells in the alveolar ducts. Our findings identify aberrant differentiation of neonatal lung myofibroblasts and demonstrate that Yap/Taz are critical for maintaining lineage commitment.

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Heparan sulfate determines myofibroblast identity during alveolar morphogenesis (ATAC-seq)

Project description:Postnatal respiration requires the bulk formation of alveoli that produces extensive surface area for gas diffusion from epithelium to the circulatory system. Alveolar morphogenesis initiates at late gestation or postnatal stage during mammalian development and is mediated by coordination among epithelial, mesenchymal and endothelial cells. Here we show that stromal cells produce Heparan Sulfate Glycosaminoglycan (HS-GAG) to maintain a niche for alveolar development by modulating both the biophysical and biochemical cues. HS is predominantly enriched in myofibroblasts in postnatal murine lungs, and genetic ablation of HS synthase gene Ext1 in fibroblast populations results in enlarged and simplified alveolar structures. HS is selectively required for the cell identity of a subset of alveolar myofibroblasts (PDGFRαhi αSMA+) residing in the distal alveolar region, which exhibit contractile properties and maintain WNT signaling activity to support normal proliferation and differentiation of alveolar epithelial cells. HS is essential to prevent precocious apoptosis of alveolar myofibroblasts. We show that these processes are dependent upon FGF/MAPK signaling and forced activation of MAPK/ERK signaling partially corrected alveolar simplification along with restoration of alveolar myofibroblast identity and AT2 cell proliferation in HS deficient mice. These data reveal HS as an essential orchestrator for developing alveolar niche critical for generation of gas exchange units.

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