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Letters to Nature
Nature 368, 249 - 251 (17 March 1994); doi:10.1038/368249a0

Disruption of the neurotrophin-3 receptor gene trkC eliminates la muscle afferents and results in abnormal movements

Rüdiger Klein*, Inmaculada Silos-Santiago, Richard J. Smeyne*, Sergio A. Lira*, Riccardo Brambilla, Sherri Bryant*, Li Zhang, William D. Snider & Mariano Barbacid*

* Department of Molecular Biology, Bristol-Myers Squibb Pharmaceutical Research Institute, Princeton, New Jersey 08543, USA
Differentiation Programme, European Molecular Biology Laboratory, 69012 Heidelberg, Germany
Department of Neurology and Neurological Surgery, Washington University School of Medicine, St Louis, Missouri 63110, USA

THE trkC gene1,2 is expressed throughout the mammalian nervous system3-5 and encodes a series of tyrosine protein kinase isoforms that serve as receptors for neurotrophin-3 (NT3), a member of the nerve growth factor (NGF) family of neurotrophic factors2,6–8. One of these isoforms, gp145trkC/TrkC Kl, mediates the trophic properties of NT3 in cultured cells2,6–8. Here we show that homozygous mice defective for TrkC tyrosine protein kinase receptors lack la muscle afferent projections to spinal motor neurons and have fewer large myelinated axons in the dorsal root and posterior columns of the spinal cord. These mice display abnormal movements and postures, indicating that NT3/TrkC-dependent sensory neurons may play a primary role in proprioception, the sense of position and movement of the limbs.

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