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An essential role for Frizzled5 in neuronal survival in the parafascicular nucleus of the thalamus.

http://www.ncbi.nlm.nih.gov/pubmed/18509025

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.

Pubmed ID: 18509025 RIS Download

Mesh terms: Alkaline Phosphatase | Animals | Animals, Newborn | Behavior, Animal | Cell Survival | Cells, Cultured | Central Nervous System | Embryo, Mammalian | Estrogen Antagonists | Frizzled Receptors | Gene Expression Regulation, Developmental | Intralaminar Thalamic Nuclei | Mice | Mice, Transgenic | Microarray Analysis | Motor Activity | Mutation | Neurons | Receptors, G-Protein-Coupled | Signal Transduction | Tamoxifen | Transfection | Weight Gain | Wnt Proteins

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Mouse Genome Informatics (Data, Gene Annotation)

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