| First Author | Parichha A | Year | 2022 |
| Journal | Nat Commun | Volume | 13 |
| Issue | 1 | Pages | 633 |
| PubMed ID | 35110543 | Mgi Jnum | J:320719 |
| Mgi Id | MGI:6870188 | Doi | 10.1038/s41467-021-27602-z |
| Citation | Parichha A, et al. (2022) Constitutive activation of canonical Wnt signaling disrupts choroid plexus epithelial fate. Nat Commun 13(1):633 |
| abstractText | The choroid plexus secretes cerebrospinal fluid and is critical for the development and function of the brain. In the telencephalon, the choroid plexus epithelium arises from the Wnt- expressing cortical hem. Canonical Wnt signaling pathway molecules such as nuclear beta-CATENIN are expressed in the mouse and human embryonic choroid plexus epithelium indicating that this pathway is active. Point mutations in human beta-CATENIN are known to result in the constitutive activation of canonical Wnt signaling. In a mouse model that recapitulates this perturbation, we report a loss of choroid plexus epithelial identity and an apparent transformation of this tissue to a neuronal identity. Aspects of this phenomenon are recapitulated in human embryonic stem cell derived organoids. The choroid plexus is also disrupted when beta-Catenin is conditionally inactivated. Together, our results indicate that canonical Wnt signaling is required in a precise and regulated manner for normal choroid plexus development in the mammalian brain. |
