Document Detail


Semaphorin3d mediates Cx43-dependent phenotypes during fin regeneration.
MedLine Citation:
PMID:  22542598     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Gap junctions are proteinaceous channels that reside at the plasma membrane and permit the exchange of ions, metabolites, and second messengers between neighboring cells. Connexin proteins are the subunits of gap junction channels. Mutations in zebrafish cx43 cause the short fin (sof(b123)) phenotype which is characterized by short fins due to defects in length of the bony fin rays. Previous findings from our lab demonstrate that Cx43 is required for both cell proliferation and joint formation during fin regeneration. Here we demonstrate that semaphorin3d (sema3d) functions downstream of Cx43. Semas are secreted signaling molecules that have been implicated in diverse cellular functions such as axon guidance, cell migration, cell proliferation, and gene expression. We suggest that Sema3d mediates the Cx43-dependent functions on cell proliferation and joint formation. Using both in situ hybridization and quantitative RT-PCR, we validated that sema3d expression depends on Cx43 activity. Next, we found that knockdown of Sema3d recapitulates all of the sof(b123) and cx43-knockdown phenotypes, providing functional evidence that Sema3d acts downstream of Cx43. To identify the potential Sema3d receptor(s), we evaluated gene expression of neuropilins and plexins. Of these, nrp2a, plxna1, and plxna3 are expressed in the regenerating fin. Morpholino-mediated knockdown of plxna1 did not cause cx43-specific defects, suggesting that PlexinA1 does not function in this pathway. In contrast, morpholino-mediated knockdown of nrp2a caused fin overgrowth and increased cell proliferation, but did not influence joint formation. Moreover, morpholino-mediated knockdown of plxna3 caused short segments, influencing joint formation, but did not alter cell proliferation. Together, our findings reveal that Sema3d functions in a common molecular pathway with Cx43. Furthermore, functional evaluation of putative Sema3d receptors suggests that Cx43-dependent cell proliferation and joint formation utilize independent membrane-bound receptors to mediate downstream cellular phenotypes.
Authors:
Quynh V Ton; M Kathryn Iovine
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't     Date:  2012-04-20
Journal Detail:
Title:  Developmental biology     Volume:  366     ISSN:  1095-564X     ISO Abbreviation:  Dev. Biol.     Publication Date:  2012 Jun 
Date Detail:
Created Date:  2012-05-21     Completed Date:  2013-07-05     Revised Date:  2014-09-17    
Medline Journal Info:
Nlm Unique ID:  0372762     Medline TA:  Dev Biol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  195-203     Citation Subset:  IM    
Copyright Information:
Copyright © 2012 Elsevier Inc. All rights reserved.
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MeSH Terms
Descriptor/Qualifier:
Animal Fins / physiology*
Animals
Cell Movement
Cell Proliferation
Gap Junctions
Gene Knockdown Techniques
Membrane Proteins / physiology*
Nerve Growth Factors / physiology*
Regeneration
Semaphorins / physiology*
Zebrafish / physiology*
Zebrafish Proteins / physiology*
Grant Support
ID/Acronym/Agency:
HD047737/HD/NICHD NIH HHS; R01 HD047737/HD/NICHD NIH HHS; R01 HD047737-05/HD/NICHD NIH HHS; R03 HD070172/HD/NICHD NIH HHS
Chemical
Reg. No./Substance:
0/Cx43.4 protein, zebrafish; 0/Membrane Proteins; 0/Nerve Growth Factors; 0/Semaphorins; 0/Zebrafish Proteins; 0/sema3d protein, zebrafish
Comments/Corrections

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