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Receptor tyrosine phosphatase PTPγ is a regulator of spinal cord neurogenesis

Receptor tyrosine phosphatase PTPγ is a regulator of spinal cord neurogenesis
Receptor tyrosine phosphatase PTPγ is a regulator of spinal cord neurogenesis

During spinal cord development the proliferation, migration and survival of neural progenitors and precursors is tightly controlled, generating the fine spatial organisation of the cord. In order to understand better the control of these processes, we have examined the function of an orphan receptor protein tyrosine phosphatase (RPTP) PTPγ, in the developing chick spinal cord. Widespread expression of PTPγ occurs post-embryonic day 3 in the early cord and is consistent with a potential role in either neurogenesis or neuronal maturation. Using gain-of-function and loss-of-function approaches in ovo, we show that PTPγ perturbation significantly reduces progenitor proliferation rates and neuronal precursor numbers, resulting in hypoplasia of the neuroepithelium. PTPγ gain-of-function causes widespread suppression of Wnt/β-catenin-driven TCF signalling. One potential target of PTPγ may therefore be β-catenin itself, since PTPγ can dephosphorylate it in vitro, but alternative targets are also likely. PTPγ loss-of-function is not sufficient to alter TCF signalling. Instead, loss-of-function leads to increased apoptosis and defective cell-cell adhesion in progenitors and precursors. Furthermore, motor neuron precursor migration is specifically defective. PTPγ therefore regulates neurogenesis during a window of spinal cord development, with molecular targets most likely related to Wnt/β-catenin signalling, cell survival and cell adhesion.

Animals, Cell Adhesion, Cell Movement, Cell Proliferation, Chick Embryo, Electroporation, Immunoblotting, In Situ Hybridization, Motor Neurons, Neural Stem Cells, Neurogenesis, Receptor-Like Protein Tyrosine Phosphatases, Class 5, Signal Transduction, Spinal Cord, Wnt Proteins, beta Catenin, Journal Article, Research Support, Non-U.S. Gov't
1044-7431
469-482
Hashemi, Hamid
c0d16271-71a7-4b35-9a2c-2b2fea5cdb66
Hurley, Michael
07b0180f-8e32-4ce1-8185-e046a42ef15a
Gibson, Anna
afeeedfa-7b10-4d38-a123-6b668522ee34
Panova, Veera
a17771ce-adde-48ac-b5ce-400ee231173f
Tchetchelnitski, Viktoria
e1238257-3252-4f54-869e-ed5ed25ac42b
Barr, Alastair
2468c4c6-0b9d-41c7-ba89-7b111bab7f56
Stoker, Andrew W
b515e6a9-72cf-4f80-a2f5-5cea484c7f3f
Hashemi, Hamid
c0d16271-71a7-4b35-9a2c-2b2fea5cdb66
Hurley, Michael
07b0180f-8e32-4ce1-8185-e046a42ef15a
Gibson, Anna
afeeedfa-7b10-4d38-a123-6b668522ee34
Panova, Veera
a17771ce-adde-48ac-b5ce-400ee231173f
Tchetchelnitski, Viktoria
e1238257-3252-4f54-869e-ed5ed25ac42b
Barr, Alastair
2468c4c6-0b9d-41c7-ba89-7b111bab7f56
Stoker, Andrew W
b515e6a9-72cf-4f80-a2f5-5cea484c7f3f

Hashemi, Hamid, Hurley, Michael, Gibson, Anna, Panova, Veera, Tchetchelnitski, Viktoria, Barr, Alastair and Stoker, Andrew W (2011) Receptor tyrosine phosphatase PTPγ is a regulator of spinal cord neurogenesis. Molecular and Cellular Neuroscience, 46 (2), 469-482. (doi:10.1016/j.mcn.2010.11.012).

Record type: Article

Abstract

During spinal cord development the proliferation, migration and survival of neural progenitors and precursors is tightly controlled, generating the fine spatial organisation of the cord. In order to understand better the control of these processes, we have examined the function of an orphan receptor protein tyrosine phosphatase (RPTP) PTPγ, in the developing chick spinal cord. Widespread expression of PTPγ occurs post-embryonic day 3 in the early cord and is consistent with a potential role in either neurogenesis or neuronal maturation. Using gain-of-function and loss-of-function approaches in ovo, we show that PTPγ perturbation significantly reduces progenitor proliferation rates and neuronal precursor numbers, resulting in hypoplasia of the neuroepithelium. PTPγ gain-of-function causes widespread suppression of Wnt/β-catenin-driven TCF signalling. One potential target of PTPγ may therefore be β-catenin itself, since PTPγ can dephosphorylate it in vitro, but alternative targets are also likely. PTPγ loss-of-function is not sufficient to alter TCF signalling. Instead, loss-of-function leads to increased apoptosis and defective cell-cell adhesion in progenitors and precursors. Furthermore, motor neuron precursor migration is specifically defective. PTPγ therefore regulates neurogenesis during a window of spinal cord development, with molecular targets most likely related to Wnt/β-catenin signalling, cell survival and cell adhesion.

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More information

Accepted/In Press date: 17 November 2010
e-pub ahead of print date: 26 November 2010
Published date: February 2011
Additional Information: Crown Copyright © 2010. Published by Elsevier Inc. All rights reserved.
Keywords: Animals, Cell Adhesion, Cell Movement, Cell Proliferation, Chick Embryo, Electroporation, Immunoblotting, In Situ Hybridization, Motor Neurons, Neural Stem Cells, Neurogenesis, Receptor-Like Protein Tyrosine Phosphatases, Class 5, Signal Transduction, Spinal Cord, Wnt Proteins, beta Catenin, Journal Article, Research Support, Non-U.S. Gov't

Identifiers

Local EPrints ID: 416273
URI: http://eprints.soton.ac.uk/id/eprint/416273
ISSN: 1044-7431
PURE UUID: c0571fea-aac4-4774-878d-59278e015782

Catalogue record

Date deposited: 11 Dec 2017 17:30
Last modified: 13 Mar 2019 19:08

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