| First Author | Hou Z | Year | 2019 |
| Journal | Development | Volume | 146 |
| Issue | 3 | PubMed ID | 30696710 |
| Mgi Jnum | J:272569 | Mgi Id | MGI:6284082 |
| Doi | 10.1242/dev.171496 | Citation | Hou Z, et al. (2019) Wnt/Fgf crosstalk is required for the specification of basal cells in the mouse trachea. Development 146(3):dev171496 |
| abstractText | Basal progenitor cells are crucial for the establishment and maintenance of the tracheal epithelium. However, it remains unclear how these progenitor cells are specified during foregut development. Here, we found that ablation of the Wnt chaperone protein Gpr177 (also known as Wntless) in mouse tracheal epithelium causes a significant reduction in the number of basal progenitor cells accompanied by cartilage loss in Shh-Cre;Gpr177(loxp/loxp) mutants. Consistent with the association between cartilage and basal cell development, Nkx2.1(+)p63(+) basal cells are co-present with cartilage nodules in Shh-Cre;Ctnnb1(DM/loxp) mutants, which maintain partial cell-cell adhesion but not the transcription regulation function of beta-catenin. More importantly, deletion of Ctnnb1 in the mesenchyme leads to the loss of basal cells and cartilage, concomitant with reduced transcript levels of Fgf10 in Dermo1-Cre;Ctnnb1(loxp/loxp) mutants. Furthermore, deletion of Fgf receptor 2 (Fgfr2) in the epithelium also leads to significantly reduced numbers of basal cells, supporting the importance of Wnt/Fgf crosstalk in early tracheal development. |
