AI Article Synopsis
- The study investigates the role of Frizzled5 (Fzd5), a receptor in the Wnt signaling pathway, in maintaining the health and function of intestinal epithelial cells.
- Deleting Fzd5 in specific intestinal stem cells impairs their ability to renew and generate new cells, affecting different aspects of epithelial structure but not overall integrity.
- Comprehensive analysis reveals that Fzd5 regulates gene expression by influencing chromatin accessibility in stem and progenitor cells, highlighting its crucial function in intestinal epithelial plasticity.
Article Abstract
The homeostasis of the intestinal epithelium relies on intricate yet insufficiently understood mechanisms of intestinal epithelial plasticity. Here, we elucidate the pivotal role of Frizzled5 (Fzd5), a Wnt pathway receptor, as a determinant of murine intestinal epithelial cell fate. Deletion of Fzd5 in Lgr5 intestinal stem cells (ISCs) impairs their self-renewal, whereas its deletion in Krt19 cells disrupts lineage generation, without affecting crypt integrity in either case. However, a broader deletion of Fzd5 across the epithelium leads to substantial crypt deterioration. Integrated analysis of single-cell RNA sequencing (scRNA-seq) and single-cell ATAC-seq (scATAC-seq) identifies that Fzd5 governs chromatin accessibility, orchestrating the regulation of stem- and lineage-related gene expression mainly in ISCs and progenitor cells. In summary, our findings provide insights into the regulatory role of Fzd5 in governing intestinal epithelial plasticity.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1016/j.devcel.2024.10.021 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Want AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!