Development · 2002 · 49 citations · 38 references
Life SciencesDevelopmental BiologyNeuroscienceDevelopmental NeuroscienceMorphogenesisSignal TransductionCell Fate DeterminationNeural DevelopmentProtein Kinase CascadesReceptor Tyrosine Kinase SignalingKinase DomainsNeurotrophin Signaling In DevelopmentReceptorsTransient ExpressionTrk Receptor SignalingTrka SignalingTrkc SignalingTyrosine Kinase Receptors
This study demonstrates that innervation dependent on two different neurotrophin tyrosine kinase (trk) receptors can form the same types of sensory endings (Merkel endings) in the same target (Merkel cells of vibrissa follicles). Some endings transiently express trkA during their initial development, whereas others express trkC throughout their development. Consequently, elimination of kinase domains of either trkA or trkC each result in a partial loss of Merkel endings, whereas absence of kinase domains of both receptors results in a total loss. At the onset of Merkel ending development, at least one kinase-lacking trkC isoform is transiently expressed on all the follicle cells, while neurotrophin 3 is transiently expressed only in the cells at the middle third of the follicle where the Merkel endings and cells develop. This transient non-neuronal expression of truncated trkC is essential for development of any Merkel endings, whereas some Merkel endings and cells still begin to develop in the absence of neurotrophin 3. Therefore, truncated trkC plays a more important role in the development of this innervation than kinase forms of trkA or trkC or of NT3, the only known ligand for trkC receptors.
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Severe sensory and sympathetic neuropathies in mice carrying a disrupted Trk/NGF receptor gene
Richard J. Smeyne, Rüdiger Klein, Andreas Schnapp et al. · Nature · 1994 · 981 citations
Medicine, Neurology, Neuroscience +16
Severe sensory and sympathetic deficits in mice lacking neurotrophin-3
Isabel Fariñas, Kevin R. Jones, Carey Backus et al. · Nature · 1994 · 640 citations