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in the optic tectum has revealed that axonal filopodia and branches arise
from sites of the axon that contain accumulation of the synaptic vesicle
protein synaptobrevin II ( Alsina et al., 2001 ). These observations indicate
that sites along the axon which contain presynaptic machinery may be
specialized, or preferred, for branch addition. Consistent with this notion,
molecules associated with presynaptic vesicle biology can promote the for-
mation of filopodia. Overexpression of synaptotagmin I in nonneuronal
cells, which do not normally express it, induces formation of prominent
filopodia ( Feany and Buckley, 1999 ), and overexpression of synaptotagmin I
in primary cortical neurons also increases formation of filopodia ( Johnsson
and Karlsson, 2012 ). Similarly, overexpression and depletion of synaptotag-
min I in chicken embryonic forebrain neurons increases and decreases the
number of axonal filopodia and branches, respectively, and synaptotagmin I
is found in close proximity to sites of axonal filopodial formation and also
within filopodia ( Greif et al., in press ). Collectively, these studies provide
evidence that the presynaptic vesicle release/recycling machinery has an
active role in the regulation of axonal morphology both before and during
synapse formation.
Active membrane recycling mechanism involving exo and endocytosis
has also been shown to be required for aspects of growth cone guidance to
both attractant and repellent signals. The guidance response of growth cones
to gradients of signals or contact with cells in vitro is characterized by asym-
metric regulation of the number of growth cone filopodia ( McCaig, 1986,
1989; Oakley and Tosney, 1993 ; Zheng et al., 1996 ; Yuan et al., 2003 ; Robles
et al., 2005 ). As a general rule, more and less filopodia are present on the side
of the growth cone facing a source of attractant and repellent relative to the
side facing away from the signal, respectively. Tojima et al. (2007) showed
that the calcium-dependent attraction of sensory growth cones is mediated
in part by asymmetric redistribution of vesicles, and that inhibition of the
vesicle protein VAMP2-mediated exocytosis blocked growth cone turning.
In contrast, clathrin-mediated endocytosis mediates growth cone responses
to repellent guidance signals, and the direct asymmetric manipulation of
exo/endocytosis across the growth cone can elicit growth cone turning
( Tojima et al., 2010 ). The myosin X motor has also been shown to contrib-
ute to the targeting of receptors for the chemoattractant netrin into filopo-
dia and at their tips ( Zhu et al., 2007 ) and undergo intrafilopodial motility
( Kerber et al., 2009 ). Similarly, the neurotrophin TrkB receptor undergoes
intrafilopodial traffic and colocalizes with synaptic vesicle markers ( Gomes
et al., 2006 ). Sites of exocytosis along filopodia may be determined by the
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