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Article: Axonal filopodial asymmetry induced by synaptic target

TitleAxonal filopodial asymmetry induced by synaptic target
Authors
Issue Date2011
PublisherAmerican Society for Cell Biology. The Journal's web site is located at http://www.molbiolcell.org/
Citation
Molecular Biology of the Cell, 2011, v. 22 n. 14, p. 2480-2490 How to Cite?
AbstractDuring 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.
Persistent Identifierhttp://hdl.handle.net/10722/139474
ISSN
2015 Impact Factor: 4.037
2015 SCImago Journal Rankings: 3.665
PubMed Central ID
ISI Accession Number ID
Funding AgencyGrant Number
Hong Kong Research Grants Council662108
Areas of Excellence GrantB-15/01-II
Funding Information:

This investigation was supported by Hong Kong Research Grants Council Grant 662108 and Areas of Excellence Grant B-15/01-II. We thank Robert Friesel for the Xenopus FGFR1 cDNA and W. K. Wong for the gift of recombinant bFGF during this study.

 

DC FieldValueLanguage
dc.contributor.authorLi, PPen_US
dc.contributor.authorChen, Cen_US
dc.contributor.authorLee, CWen_US
dc.contributor.authorMadhavan, Ren_US
dc.contributor.authorPeng, HBen_US
dc.date.accessioned2011-09-23T05:50:28Z-
dc.date.available2011-09-23T05:50:28Z-
dc.date.issued2011en_US
dc.identifier.citationMolecular Biology of the Cell, 2011, v. 22 n. 14, p. 2480-2490en_US
dc.identifier.issn1059-1524en_US
dc.identifier.urihttp://hdl.handle.net/10722/139474-
dc.description.abstractDuring 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.-
dc.languageengen_US
dc.publisherAmerican Society for Cell Biology. The Journal's web site is located at http://www.molbiolcell.org/-
dc.relation.ispartofMolecular Biology of the Cellen_US
dc.rightsMolecular Biology of the Cell. Copyright © American Society for Cell Biology.-
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License-
dc.subject.meshAxons - metabolism - physiology-
dc.subject.meshFibroblast Growth Factor 2 - metabolism-
dc.subject.meshNeuromuscular Junction - growth and development - metabolism-
dc.subject.meshPseudopodia - metabolism - physiology-
dc.subject.meshReceptor, Fibroblast Growth Factor, Type 1 - metabolism-
dc.titleAxonal filopodial asymmetry induced by synaptic targeten_US
dc.typeArticleen_US
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=1939-4586 (Electronic) 1059-1524 (Linkin&volume=22&issue=14&spage=2480&epage=90&date=2011&atitle=Axonal+filopodial+asymmetry+induced+by+synaptic+targeten_US
dc.identifier.emailChen, C: endocc@hku.hken_US
dc.description.naturepublished_or_final_version-
dc.identifier.doi10.1091/mbc.E11-03-0198-
dc.identifier.pmid21613540-
dc.identifier.pmcidPMC3135474-
dc.identifier.scopuseid_2-s2.0-79960290138-
dc.identifier.hkuros195022en_US
dc.identifier.volume22en_US
dc.identifier.issue14en_US
dc.identifier.spage2480en_US
dc.identifier.epage2490en_US
dc.identifier.eissn1939-4586-
dc.identifier.isiWOS:000292687800006-
dc.publisher.placeUnited States-

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