Document Detail


Semaphorin3d mediates Cx43-dependent phenotypes during fin regeneration.
MedLine Citation:
PMID:  22542598     Owner:  NLM     Status:  Publisher    
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
Related Documents :
18834508 - Anti cancer effects of curcumin: cycle of life and death.
18613038 - Optimization of yeast cell cycle analysis and morphological characterization by multisp...
21118798 - Hepatoblastoma in a cat.
12897798 - Coupling the cell cycle to cell growth.
7956398 - Assessment of an ultrathin bronchoscope that allows cytodiagnosis of small airways.
2569248 - Identification and percentage frequency of isolated non-parenchymal liver cells (nplc) ...
Publication Detail:
Type:  JOURNAL ARTICLE     Date:  2012-4-20
Journal Detail:
Title:  Developmental biology     Volume:  -     ISSN:  1095-564X     ISO Abbreviation:  -     Publication Date:  2012 Apr 
Date Detail:
Created Date:  2012-4-30     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  0372762     Medline TA:  Dev Biol     Country:  -    
Other Details:
Languages:  ENG     Pagination:  -     Citation Subset:  -    
Copyright Information:
Copyright © 2012 Elsevier Inc. All rights reserved.
Affiliation:
Department of Biological Sciences, Lehigh University, 111 Research Drive, Iacocca B-217, Bethlehem, PA 18015, United States.
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Descriptor/Qualifier:

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


Previous Document:  The CSF-1 receptor ligands IL-34 and CSF-1 exhibit distinct developmental brain expression patterns ...
Next Document:  A network of PUF proteins and Ras signaling promote mRNA repression and oogenesis in C. elegans.