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CD45+ Epcam- poluation scRNAseq analysis in control and Goblet-Y/T-Scgb1a1CreERT mouse lung tissues.

ABSTRACT: The gole of this experiment is to get an in depth understanding of the immune population responses in mouse lungs presented with goblet cell metaplasia in the airway upon Yap/Taz deletion in Scgb1a1+ cells.

ORGANISM(S): Mus musculus

PROVIDER: GSE275467 | GEO | 2025/08/20

REPOSITORIES: GEO

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scRNAseq analysis in control and Goblet-Y/T-Scgb1a1CreERT mouse lung tissues.

Project description:This experiment aims to examine the global cellular response in the lung tissues of Goblet-Y/T-Scgb1a1CreERT mice. Depletion of Yap and Taz in airway secretory cells resulted in goblet cell metaplasia. To elucidate the underlying cellular response, we utilized scRNA sequencing of lung tissues.

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Yap/Taz inhibit goblet cell fate to maintain lung epithelial homeostasis

Project description:Proper lung function relies on precisely balanced numbers of specialized epithelial cell types that work together and are maintained in homeostasis. We describe essential roles for the transcriptional regulators Yap and Taz, which are key effectors of Hippo pathway signaling, in maintaining lung epithelial homeostasis. We report that conditional deletion of Yap1/Yap and Wwtr1/Taz in the lung epithelium of adult mice results in severe defects with consequent animal lethality. Phenotypes associated with Yap/Taz deletion include alveolar defects and a striking development of goblet cell metaplasia throughout the airways. We performed gene expression analysis of wild type and Yap/Taz null primary mouse airway epithelial cells in order to define Yap/Taz controlled gene expression.

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Project description:Proper lung function relies on precisely balanced numbers of specialized epithelial cell types that work together and are maintained in homeostasis. In this study we have described essential roles for the transcriptional regulators YAP and TAZ, which are key effectors of Hippo pathway signaling, in maintaining lung epithelial homeostasis. Phenotypes associated with Yap/Taz deletion include alveolar defects and a striking development of goblet cell metaplasia throughout the airways. Lineage specific deletion of Yap and Taz in Scgb1a1+ cells leads to increased Mucin production within the knockout cells in vivo. In order better characterize the in vivo transcriptional changes associated with Yap/Taz knockout in these cells, we have isolated Scgb1a1 lineage traced cells from control and yap/taz cNull mice and performed bulk RNA sequencing.

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Project description:Proper lung function relies on precisely balanced numbers of specialized epithelial cell types that work together and are maintained in homeostasis. In this study we have described essential roles for the transcriptional regulators YAP and TAZ, which are key effectors of Hippo pathway signaling, in maintaining lung epithelial homeostasis. Phenotypes associated with Yap/Taz deletion include alveolar defects and a striking development of goblet cell metaplasia throughout the airways. Knockdown of YAP and TAZ in HBECs similarly drives mucin expression. The TEAD family of transcription factors are well characterized partners of the YAP/TAZ transcriptional effectors, and we have found that knockdown of TEAD1-4 similarly drives elevated mucin expression. In order to further understand the role of the TEAD transcription factors in human lung epithelial cell fate, we conducted TEAD Chromatin Immunopreciptitation (ChIP)-Sequencing.

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