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Vol. 14, No. 17, pp. 2216-2228, September 1, 2000
Laboratory of Developmental Neurobiology, The Rockefeller
University, New York, New York 10021-6399 USA
In the developing cerebellum, granule neuron axon outgrowth is a key
step toward establishing proper connections with Purkinje neurons, the
principal output neuron of the cerebellum. During a search for genes
that function in this process, we identified a receptor tyrosine kinase
discoidin domain receptor 1 (DDR1) expressed in granule cells
throughout their development. Overexpression of a dominant-negative
form of DDR1 in immature granule cells results in severe reduction of
neurite outgrowth in vitro, in dissociated primary culture, and in
vivo, in organotypic slices of neonatal cerebellum. Granule cells that
fail to extend axons are positive for differentiation markers such as
TAG-1 and the neuron-specific class III 
-tubulin, suggesting that
development is affected after granule cells commit to terminal
differentiation. DDR1 activation appears to be mediated by its ligand,
collagen, which is localized to the pial layer of the developing
cerebellum, thereby leading to granule cell parallel fiber extension.
Our results therefore indicate that collagen-DDR1 signaling is
essential for granule neuron axon formation and further suggest a
unique role of pia in cerebellar cortex histogenesis.
[Key Words: DDR; collagen; parallel fiber; axon extension; cerebellar granule neuron; retrovirus]
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