Forced Notch Signaling Inhibits Commissural Axon Outgrowth in the Developing Chick Central Nerve System

Hdl Handle:
http://hdl.handle.net/10675.2/627
Title:
Forced Notch Signaling Inhibits Commissural Axon Outgrowth in the Developing Chick Central Nerve System
Authors:
Shi, Ming; Liu, Zhirong; Lv, Yonggang; Zheng, Minhua; Du, Fang; Zhao, Gang; Huang, Ying; Chen, Jiayin; Han, Hua; Ding, Yuqiang
Abstract:
Background: A collection of in vitro evidence has demonstrated that Notch signaling plays a key role in the growth of neurites in differentiated neurons. However, the effects of Notch signaling on axon outgrowth in an in vivo condition remain largely unknown.; Methodology/Principal Findings: In this study, the neural tubes of HH10-11 chick embryos were in ovo electroporated with various Notch transgenes of activating or inhibiting Notch signaling, and then their effects on commissural axon outgrowth across the floor plate midline in the chick developing central nerve system were investigated. Our results showed that forced expression of Notch intracellular domain, constitutively active form of RBPJ, or full-length Hes1 in the rostral hindbrain, diencephalon and spinal cord at stage HH10-11 significantly inhibited commissural axon outgrowth. On the other hand, inhibition of Notch signaling by ectopically expressing a dominant-negative form of RBPJ promoted commissural axonal growth along the circumferential axis. Further results revealed that these Notch signaling-mediated axon outgrowth defects may be not due to the alteration of axon guidance since commissural axon marker TAG1 was present in the axons in floor plate midline, and also not result from the changes in cell fate determination of commissural neurons since the expression of postmitotic neuron marker Tuj1 and specific commissural markers TAG1 and Pax7 was unchanged.; Conclusions/Significance: We first used an in vivo system to provide evidence that forced Notch signaling negatively regulates commissural axon outgrowth.
Editors:
Mei, Lin
Citation:
PLoS One. 2011 Jan 21; 6(1):e14570
Issue Date:
21-Jan-2011
URI:
http://hdl.handle.net/10675.2/627
DOI:
10.1371/journal.pone.0014570
PubMed ID:
21283742
PubMed Central ID:
PMC3024975
Type:
Article
ISSN:
1932-6203
Appears in Collections:
Department of Neurology: Faculty Research and Presentations

Full metadata record

DC FieldValue Language
dc.contributor.authorShi, Mingen_US
dc.contributor.authorLiu, Zhirongen_US
dc.contributor.authorLv, Yonggangen_US
dc.contributor.authorZheng, Minhuaen_US
dc.contributor.authorDu, Fangen_US
dc.contributor.authorZhao, Gangen_US
dc.contributor.authorHuang, Yingen_US
dc.contributor.authorChen, Jiayinen_US
dc.contributor.authorHan, Huaen_US
dc.contributor.authorDing, Yuqiangen_US
dc.contributor.editorMei, Lin-
dc.date.accessioned2012-10-26T16:26:55Z-
dc.date.available2012-10-26T16:26:55Z-
dc.date.issued2011-01-21en_US
dc.identifier.citationPLoS One. 2011 Jan 21; 6(1):e14570en_US
dc.identifier.issn1932-6203en_US
dc.identifier.pmid21283742en_US
dc.identifier.doi10.1371/journal.pone.0014570en_US
dc.identifier.urihttp://hdl.handle.net/10675.2/627-
dc.description.abstractBackground: A collection of in vitro evidence has demonstrated that Notch signaling plays a key role in the growth of neurites in differentiated neurons. However, the effects of Notch signaling on axon outgrowth in an in vivo condition remain largely unknown.en_US
dc.description.abstractMethodology/Principal Findings: In this study, the neural tubes of HH10-11 chick embryos were in ovo electroporated with various Notch transgenes of activating or inhibiting Notch signaling, and then their effects on commissural axon outgrowth across the floor plate midline in the chick developing central nerve system were investigated. Our results showed that forced expression of Notch intracellular domain, constitutively active form of RBPJ, or full-length Hes1 in the rostral hindbrain, diencephalon and spinal cord at stage HH10-11 significantly inhibited commissural axon outgrowth. On the other hand, inhibition of Notch signaling by ectopically expressing a dominant-negative form of RBPJ promoted commissural axonal growth along the circumferential axis. Further results revealed that these Notch signaling-mediated axon outgrowth defects may be not due to the alteration of axon guidance since commissural axon marker TAG1 was present in the axons in floor plate midline, and also not result from the changes in cell fate determination of commissural neurons since the expression of postmitotic neuron marker Tuj1 and specific commissural markers TAG1 and Pax7 was unchanged.en_US
dc.description.abstractConclusions/Significance: We first used an in vivo system to provide evidence that forced Notch signaling negatively regulates commissural axon outgrowth.en_US
dc.rightsShi et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.en_US
dc.subjectResearch Articleen_US
dc.subjectDevelopmental Biology/Neurodevelopmenten_US
dc.subjectNeuroscience/Neurobiology of Disease and Regenerationen_US
dc.subjectNeuroscience/Neurodevelopmenten_US
dc.titleForced Notch Signaling Inhibits Commissural Axon Outgrowth in the Developing Chick Central Nerve Systemen_US
dc.typeArticleen_US
dc.identifier.pmcidPMC3024975en_US
dc.contributor.corporatenameDepartment of Neurology-

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