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Axonal filopodial asymmetry induced by synaptic target

Authors Li, Pan P. HKUST affiliated (currently or previously)
Chen, Cheng
Lee, Chi-Wai HKUST affiliated (currently or previously)
Madhavan, Raghavan HKUST affiliated (currently or previously)
Peng, H. Benjamin View this author's profile
Issue Date 2011
Source Molecular biology of the cell , v. 22, (14), July 2011, p. 2480-2490
Summary During vertebrate neuromuscular junction (NMJ) assembly, motor axons and their muscle targets exchange short-range signals that regulate the subsequent steps of presynaptic and postsynaptic specialization. We report here that this interaction is in part mediated by axonal filopodia extended preferentially by cultured Xenopus spinal neurons toward their muscle targets. Immunoblotting and labeling experiments showed that basic fibroblast growth factor (bFGF) was expressed by muscle and associated with the cell surface, and treatment of cultured spinal neurons with recombinant bFGF nearly doubled the normal density of filopodia in neurites. This effect of bFGF was abolished by SU5402, a selective inhibitor of FGF-receptor 1 (FGFR1), and forced expression of wild-type or dominant-negative FGFR1 in neurons enhanced or suppressed the assembly of filopodia, respectively. Significantly, in nerve-muscle cocultures, knocking down bFGF in muscle decreased both the asymmetric extension of filopodia by axons toward muscle and the assembly of NMJs. In addition, neurons expressing dominant-negative FGFR1 less effectively triggered the aggregation of muscle acetylcholine receptors at innervation sites than did control neurons. These results suggest that bFGF activation of neuronal FGFR1 generates filopodial processes in neurons that promote nerve-muscle interaction and facilitate NMJ establishment.
ISSN 1059-1524
Rights Copyright © 2011 The Amercian Society for Cell Biology
Language English
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