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

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

Authors

  • Liu C
  • Wang Y
  • Smallwood PM
  • Nathans J

Journal

The Journal of neuroscience : the official journal of the Society for Neuroscience

Publication Data

May 28, 2008

Associated Grants

None

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