期刊
CELL
卷 184, 期 14, 页码 3702-+出版社
CELL PRESS
DOI: 10.1016/j.cell.2021.05.015
关键词
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资金
- NIH Intramural Research Program (NIDCR) [ZIA DE000525]
- NIH Intramural Research Program (NIBIB) [ZIA EB000094]
- NIH Distinguished Scholars Program
- NIDCR K99 Pathway to Independence Award [K99 DE27982]
The study found that in embryonic salivary glands, budding morphogenesis is driven by the expansion and folding of a specific epithelial surface cell sheet characterized by strong cell-matrix adhesions and weak cell-cell adhesions. Experimental validation showed that cell-matrix adhesion is essential for budding morphogenesis.
Many embryonic organs undergo epithelial morphogenesis to form tree-like hierarchical structures. However, it remains unclear what drives the budding and branching of stratified epithelia, such as in the embryonic salivary gland and pancreas. Here, we performed live-organ imaging of mouse embryonic salivary glands at single-cell resolution to reveal that budding morphogenesis is driven by expansion and folding of a distinct epithelial surface cell sheet characterized by strong cell-matrix adhesions and weak cell-cell adhesions. Profiling of single-cell transcriptomes of this epithelium revealed spatial patterns of transcription underlying these cell adhesion differences. We then synthetically reconstituted budding morphogenesis by experimentally suppressing E-cadherin expression and inducing basement membrane formation in 3D spheroid cultures of engineered cells, which required beta 1-integrin-mediated cell-matrix adhesion for successful budding. Thus, stratified epithelial budding, the key first step of branching morphogenesis, is driven by an overall combination of strong cell-matrix adhesion and weak cell-cell adhesion by peripheral epithelial cells.
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