Document Detail


Promotion of proliferation in the developing cerebral cortex by EphA4 forward signaling.
MedLine Citation:
PMID:  19542359     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Eph receptors are widely expressed during cerebral cortical development, yet a role for Eph signaling in the generation of cells during corticogenesis has not been shown. Cortical progenitor cells selectively express one receptor, EphA4, and reducing EphA4 signaling in cultured progenitors suppressed proliferation, decreasing cell number. In vivo, EphA4(-/-) cortex had a reduced area, fewer cells and less cell division compared with control cortex. To understand the effects of EphA4 signaling in corticogenesis, EphA4-mediated signaling was selectively depressed or elevated in cortical progenitors in vivo. Compared with control cells, cells with reduced EphA4 signaling were rare and mitotically inactive. Conversely, overexpression of EphA4 maintained cells in their progenitor states at the expense of subsequent maturation, enlarging the progenitor pool. These results support a role for EphA4 in the autonomous promotion of cell proliferation during corticogenesis. Although most ephrins were undetectable in cortical progenitors, ephrin B1 was highly expressed. Our analyses demonstrate that EphA4 and ephrin B1 bind to each other, thereby initiating signaling. Furthermore, overexpression of ephrin B1 stimulated cell division of neighboring cells, supporting the hypothesis that ephrin B1-initiated forward signaling of EphA4 promotes cortical cell division.
Authors:
Hilary A North; Xiumei Zhao; Sharon M Kolk; Meredith A Clifford; Daniela M Ziskind; Maria J Donoghue
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Development (Cambridge, England)     Volume:  136     ISSN:  0950-1991     ISO Abbreviation:  Development     Publication Date:  2009 Jul 
Date Detail:
Created Date:  2009-06-22     Completed Date:  2009-09-24     Revised Date:  2010-07-02    
Medline Journal Info:
Nlm Unique ID:  8701744     Medline TA:  Development     Country:  England    
Other Details:
Languages:  eng     Pagination:  2467-76     Citation Subset:  IM    
Affiliation:
Department of Biology, Georgetown University, 334 Reiss Science Building, Washington, DC 20057, USA.
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MeSH Terms
Descriptor/Qualifier:
Animals
Cell Communication
Cell Proliferation
Cells, Cultured
Cerebral Cortex / cytology,  embryology*,  metabolism*
Embryonic Stem Cells / cytology,  metabolism
Ephrin-B1 / genetics,  metabolism
Female
Gene Expression Regulation, Developmental
Ligands
Mice
Mice, Inbred C57BL
Mice, Knockout
Models, Neurological
Pregnancy
Receptor, EphA4 / deficiency,  genetics,  metabolism*
Recombinant Proteins / genetics,  metabolism
Signal Transduction
Grant Support
ID/Acronym/Agency:
5T32DA00729/DA/NIDA NIH HHS; R01 NS 9979-02/NS/NINDS NIH HHS; T32 NS041231-09/NS/NINDS NIH HHS; T32NS041231/NS/NINDS NIH HHS
Chemical
Reg. No./Substance:
0/Efnb1 protein, mouse; 0/Ephrin-B1; 0/Ligands; 0/Recombinant Proteins; EC 2.7.10.1/Receptor, EphA4
Comments/Corrections

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