| First Author | Zhu S | Year | 2024 |
| Journal | iScience | Volume | 27 |
| Issue | 9 | Pages | 110785 |
| PubMed ID | 39286503 | Mgi Jnum | J:354246 |
| Mgi Id | MGI:7732893 | Doi | 10.1016/j.isci.2024.110785 |
| Citation | Zhu S, et al. (2024) Follistatin controls the number of murine teeth by limiting TGF-beta signaling. iScience 27(9):110785 |
| abstractText | Supernumerary teeth are common developmental anomalies of dentition. However, the factors and mechanisms driving their formation remain largely unknown. Here, we report that conditional knockout of Fst, encoding an antagonist for the transforming growth factor beta (TGF-beta) signaling pathway, in both oral epithelium and mesenchyme of mice (Fst (CKO) ) led to supernumerary upper incisor teeth, arising from the lingual dental epithelium of the native teeth and preceded by an enlarged and split lingual cervical loop. Fst-deficiency greatly activated TGF-beta signaling in developing maxillary incisor teeth, associated with increased epithelium cell proliferation. Moreover, Fst (CKO) teeth exhibited increased expression of Tbx1, Sp6, and Sox2, which were identified as direct targets of TGF-beta/SMAD2 signaling. Finally, we show that upregulation of Tbx1 in response to Fst-deficiency was largely responsible for the formation of extra teeth in Fst (CKO) mice. Taken together, our investigation indicates a novel role for Fst in controlling murine tooth number by restricting TGF-beta signaling. |
