In this research, I explored the role of FOXL1+ telocytes in the maintenance of intestinal stem cells (ISCs). These telocytes were identified as a critical source of both Wnt activators and inhibitors, localized strategically along the crypt-villus axis to regulate the Wnt signaling environment within the intestinal stem cell niche.

To investigate this, our group generated a mouse model for conditional ablation of Porcupine (a protein necessary for Wnt ligand maturation) specifically in FOXL1+ cells using a tamoxifen-inducible Cre-lox system. Using this model, we demonstrated that Wnt secretion from FoxL1+ cells is indispensable for epithelial renewal, as its loss caused decreased nuclear β-catenin, a marker of active Wnt signaling, as well as decreased ISC markers and impaired epithelial proliferation. 

My role in this project was to perform immunohistochemical (IHC) staining and conduct quantitative analyses of single-molecule fluorescence in situ hybridization (smFISH) experiments. IHC was utilized to localize proteins such as β-catenin and cyclin D1, while smFISH was used to spatially and quantitatively map the expression of key Wnt signaling molecules such as Wnt2b and Rspo3. These efforts contributed to the crucial evidence of the spatial compartmentalization of Wnt ligands and the signaling disruptions caused by Porcupine ablation in FoxL1+ cells. This work underscores the importance of FOXL1+ telocytes in maintaining the intestinal stem cell niche and epithelial homeostasis.