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PI3K Signaling Specifies Proximal-Distal Fate by Driving a Developmental Gene Regulatory Network in SOX9+ Lung Progenitors

ABSTRACT: PI3K Signaling Specifies Proximal-Distal Fate by Driving a Developmental Gene Regulatory Network in SOX9+ Lung Progenitors

PROVIDER: PRJNA777958 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR16775625_1.fastq.gz	Fastqsanger.gz
	SRR16775625_2.fastq.gz	Fastqsanger.gz
	SRR16775626_1.fastq.gz	Fastqsanger.gz
	SRR16775626_2.fastq.gz	Fastqsanger.gz
	SRR16775627_1.fastq.gz	Fastqsanger.gz

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PI3K Signaling Specifies Proximal-Distal Fate by Driving a Developmental Gene Regulatory Network in SOX9+ Lung Progenitors [ATAC-seq]

Project description:PI3K Signaling Specifies Proximal-Distal Fate by Driving a Developmental Gene Regulatory Network in SOX9+ Lung Progenitors [ATAC-seq]

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PI3K Signaling Specifies Proximal-Distal Fate by Driving a Developmental Gene Regulatory Network in SOX9+ Lung Progenitors [RNA-seq]

Project description:PI3K Signaling Specifies Proximal-Distal Fate by Driving a Developmental Gene Regulatory Network in SOX9+ Lung Progenitors [RNA-seq]

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PI3K Signaling Specifies Proximal-Distal Fate by Driving a Developmental Gene Regulatory Network in SOX9+ Lung Progenitors [ATAC-seq]

Project description:In order to understand the epigenetic mechanisms directing development and differentiation of SOX9+ lung epithelial progenitor cells (EPCs), paired RNA-Seq and ATAC-Seq was performed on SOX9+ EPCs sorted using flow cytometry from a Sox9-GFP reporter mouse.

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PI3K Signaling Specifies Proximal-Distal Fate by Driving a Developmental Gene Regulatory Network in SOX9+ Lung Progenitors [RNA-seq]

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PI3K signaling specifies proximal-distal fate by driving a developmental gene regulatory network in SOX9+ mouse lung progenitors.

Project description:The tips of the developing respiratory buds are home to important progenitor cells marked by the expression of SOX9 and ID2. Early in embryonic development (prior to E13.5), SOX9+progenitors are multipotent, generating both airway and alveolar epithelium, but are selective progenitors of alveolar epithelial cells later in development. Transcription factors, including Sox9, Etv5, Irx, Mycn, and Foxp1/2 interact in complex gene regulatory networks to control proliferation and differentiation of SOX9+progenitors. Molecular mechanisms by which these transcription factors and other signaling pathways control chromatin state to establish and maintain cell-type identity are not well-defined. Herein, we analyze paired gene expression (RNA-Seq) and chromatin accessibility (ATAC-Seq) data from SOX9+ epithelial progenitor cells (EPCs) during embryonic development in Mus musculus. Widespread changes in chromatin accessibility were observed between E11.5 and E16.5, particularly at distal cis-regulatory elements (e.g. enhancers). Gene regulatory network (GRN) inference identified a common SOX9+ progenitor GRN, implicating phosphoinositide 3-kinase (PI3K) signaling in the developmental regulation of SOX9+ progenitor cells. Consistent with this model, conditional ablation of PI3K signaling in the developing lung epithelium in mouse resulted in an expansion of the SOX9+ EPC population and impaired airway epithelial cell differentiation. These data demonstrate that PI3K signaling is required for epithelial patterning during lung organogenesis, and emphasize the combinatorial power of paired RNA and ATAC seq in defining regulatory networks in development.

| S-EPMC9427112 | biostudies-literature

PI3K Signaling Specifies Proximal-Distal Fate by Driving a Developmental Gene Regulatory Network in SOX9+ Lung Progenitors

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

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Project description:The steps governing healing with or without fibrosis within the same microenvironment are unclear. After acute kidney injury (AKI), the injured proximal tubular epithelial cells activate Sox9 for self-restoration. Using head-to-head comparison of injury- induced Sox9-lineages via spatiotemporal mapping, single-cell sequencing, and single-nuclei chromatin accessibility profiling, we identified a dynamic SOX9 switch. Lineages that regenerated epithelia silenced SOX9 and healed without fibrosis (SOX9on-off). In contrast, lineages that maintained Sox9 activity in attempt to regenerate, demarcated by SOX9-induced Cadherin 6 (SOX9on-on CDH6pos ) cell state, generated single-cell Wnt activity to provoke a fibroproliferative response in adjacent fibroblasts, driving AKI to chronic kidney disease. Transplanted human kidneys displayed similar SOX9/CDH6/WNT2B responses post-injury. Thus, we uncovered a mechanism linking fibrosis to sustained efforts to regenerate the injured tissue.

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