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The receptor tyrosine kinase MuSK is required for neuromuscular junction formation in vivo.

Formation of neuromuscular synapses requires a series of inductive interactions between growing motor axons and differentiating muscle cells, culminating in the precise juxtaposition of a highly specialized nerve terminal with a complex molecular structure on the postsynaptic muscle surface. The receptors and signaling pathways mediating these inductive interactions are not known. We have generated mice with a targeted disruption of the gene encoding MuSK, a receptor tyrosine kinase selectively localized to the postsynaptic muscle surface. Neuromuscular synapses do not form in these mice, suggesting a failure in the induction of synapse formation. Together with the results of an accompanying manuscript, our findings indicate that MuSK responds to a critical nerve-derived signal (agrin), and in turn activates signaling cascades responsible for all aspects of synapse formation, including organization of the postsynaptic membrane, synapse-specific transcription, and presynaptic differentiation.

Pubmed ID: 8653786

Authors

  • DeChiara TM
  • Bowen DC
  • Valenzuela DM
  • Simmons MV
  • Poueymirou WT
  • Thomas S
  • Kinetz E
  • Compton DL
  • Rojas E
  • Park JS
  • Smith C
  • DiStefano PS
  • Glass DJ
  • Burden SJ
  • Yancopoulos GD

Journal

Cell

Publication Data

May 17, 1996

Associated Grants

  • Agency: NINDS NIH HHS, Id: NS21579
  • Agency: NINDS NIH HHS, Id: NS27963
  • Agency: NINDS NIH HHS, Id: R01 NS036193
  • Agency: NINDS NIH HHS, Id: R01 NS036193-01A1S1

Mesh Terms

  • Agrin
  • Animals
  • Animals, Newborn
  • Cell Differentiation
  • Gene Deletion
  • Gene Expression
  • Genes, Lethal
  • Mice
  • Mice, Knockout
  • Muscle Fibers, Skeletal
  • Muscle, Skeletal
  • Neuromuscular Junction
  • Receptor Protein-Tyrosine Kinases
  • Receptors, Cholinergic
  • Signal Transduction
  • Synapses
  • Synaptic Membranes
  • Transcription, Genetic