| First Author | Liu C | Year | 2008 |
| Journal | J Neurosci | Volume | 28 |
| Issue | 22 | Pages | 5641-53 |
| PubMed ID | 18509025 | Mgi Jnum | J:136390 |
| Mgi Id | MGI:3796265 | Doi | 10.1523/JNEUROSCI.1056-08.2008 |
| Citation | Liu C, et al. (2008) An essential role for Frizzled5 in neuronal survival in the parafascicular nucleus of the thalamus. J Neurosci 28(22):5641-53 |
| abstractText | Frizzled5 (Fz5), a putative Wnt receptor, is expressed in the retina, hypothalamus, and the parafascicular nucleus (PFN) of the thalamus. By constructing Fz5 alleles in which beta-galactosidase replaces Fz5 or in which Cre-mediated recombination replaces Fz5 with alkaline phosphatase, we observe that Fz5 is required continuously and in a cell autonomous manner for the survival of adult PFN neurons, but is not required for proliferation, migration, or axonal growth and targeting of developing PFN neurons. A motor phenotype associated with loss of Fz5 establishes a role for the PFN in sensorimotor coordination. Transcripts coding for Wnt9b, the likely Fz5 ligand in vivo, and beta-catenin, a mediator of canonical Wnt signaling, are both downregulated in the Fz5(-/-) PFN, implying a positive feedback mechanism in which Wnt signaling is required to maintain the expression of Wnt signaling components. These data suggest that defects in Wnt-Frizzled signaling could be the cause of neuronal loss in degenerative CNS diseases. |
