Forced notch signaling inhibits commissural axon outgrowth in the developing chick central nerve system.

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...

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Main Authors: Ming Shi, Zhirong Liu, Yonggang Lv, Minhua Zheng, Fang Du, Gang Zhao, Ying Huang, Jiayin Chen, Hua Han, Yuqiang Ding
Format: Article
Language:English
Published: Public Library of Science (PLoS) 2011-01-01
Series:PLoS ONE
Online Access:http://europepmc.org/articles/PMC3024975?pdf=render
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author Ming Shi
Zhirong Liu
Yonggang Lv
Minhua Zheng
Fang Du
Gang Zhao
Ying Huang
Jiayin Chen
Hua Han
Yuqiang Ding
author_facet Ming Shi
Zhirong Liu
Yonggang Lv
Minhua Zheng
Fang Du
Gang Zhao
Ying Huang
Jiayin Chen
Hua Han
Yuqiang Ding
author_sort Ming Shi
collection DOAJ
description 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.
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spelling doaj.art-1af1409a3efd4674895d07d24501530a2022-12-21T18:20:05ZengPublic Library of Science (PLoS)PLoS ONE1932-62032011-01-0161e1457010.1371/journal.pone.0014570Forced notch signaling inhibits commissural axon outgrowth in the developing chick central nerve system.Ming ShiZhirong LiuYonggang LvMinhua ZhengFang DuGang ZhaoYing HuangJiayin ChenHua HanYuqiang DingBACKGROUND: 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.http://europepmc.org/articles/PMC3024975?pdf=render
spellingShingle Ming Shi
Zhirong Liu
Yonggang Lv
Minhua Zheng
Fang Du
Gang Zhao
Ying Huang
Jiayin Chen
Hua Han
Yuqiang Ding
Forced notch signaling inhibits commissural axon outgrowth in the developing chick central nerve system.
PLoS ONE
title Forced notch signaling inhibits commissural axon outgrowth in the developing chick central nerve system.
title_full Forced notch signaling inhibits commissural axon outgrowth in the developing chick central nerve system.
title_fullStr Forced notch signaling inhibits commissural axon outgrowth in the developing chick central nerve system.
title_full_unstemmed Forced notch signaling inhibits commissural axon outgrowth in the developing chick central nerve system.
title_short Forced notch signaling inhibits commissural axon outgrowth in the developing chick central nerve system.
title_sort forced notch signaling inhibits commissural axon outgrowth in the developing chick central nerve system
url http://europepmc.org/articles/PMC3024975?pdf=render
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