Document Detail


Opposing functions of ATF2 and Fos-like transcription factors in c-Jun-mediated myogenin expression and terminal differentiation of avian myoblasts.
MedLine Citation:
PMID:  11753683     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
With the aim to identify the oncoprotein partners implicated in the c-Jun myogenic influence, we carried out stable transfection experiments of c-Jun and/or ATF2, Fra2, c-Fos overexpression in avian myoblasts. Before induction of differentiation, c-Jun repressed myoblast withdrawal from the cell cycle, as did a TPA treatment. However, after serum removal, unlike TPA, c-Jun significantly stimulated myoblast differentiation. In search for specific partners involved in this dual influence, we found that a reduction in the amounts of c-Fos and Fra2 and an increase in c-Jun proteins occurred at cell confluence, a situation likely to favor cooperation between c-Jun and ATF2 during terminal differentiation. Whereas c-Fos and Fra2 cooperated with c-Jun to abrogate myoblast withdrawal from the cell cycle and terminal differentiation, ATF2 co-expression potentiated the positive myogenic c-Jun influence. In addition, myogenin expression was a positive target of this cooperation and this regulation occurred through a stimulation of myogenin promoter activity: (1) whereas c-Fos or Fra2 co-expression abrogated c-Jun stimulatory activity on this promoter, ATF2 co-expression potentiated this influence; (2) using a dominant negative ATF2 mutant, we established that c-Jun transcriptional activity required functionality of endogenous ATF2. These data suggest that through this dual myogenic influence due to cooperations with different partners, c-Jun is involved in the control of duration of myoblast proliferation and thereafter of fusion efficiency.
Authors:
L Daury; M Busson; N Tourkine; F Casas; I Cassar-Malek; C Wrutniak-Cabello; M Castellazzi; G Cabello
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Oncogene     Volume:  20     ISSN:  0950-9232     ISO Abbreviation:  Oncogene     Publication Date:  2001 Nov 
Date Detail:
Created Date:  2001-12-25     Completed Date:  2002-01-10     Revised Date:  2008-11-21    
Medline Journal Info:
Nlm Unique ID:  8711562     Medline TA:  Oncogene     Country:  England    
Other Details:
Languages:  eng     Pagination:  7998-8008     Citation Subset:  IM    
Affiliation:
Unité d'Endocrinologie Cellulaire, UMR Différenciation Cellulaire et Croissance, Institut National de la Recherche Agronomique (INRA), 2 place Viala, 34060 Montpellier Cedex 1, France.
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MeSH Terms
Descriptor/Qualifier:
Activating Transcription Factor 2
Animals
Blotting, Western
Cell Cycle
Cell Differentiation*
Cell Division
Cell Line
Cyclic AMP Response Element-Binding Protein / genetics,  metabolism*
DNA-Binding Proteins / metabolism
Dimerization
Fos-Related Antigen-2
Genes, Dominant
Microscopy, Fluorescence
Muscles / cytology*,  metabolism
Mutation
Myogenin / genetics,  metabolism*
Promoter Regions, Genetic / genetics
Proto-Oncogene Proteins c-fos / metabolism*
Proto-Oncogene Proteins c-jun / metabolism*
Quail*
RNA, Messenger / genetics,  metabolism
Transcription Factor AP-1 / metabolism
Transcription Factors / genetics,  metabolism*
Transfection
Chemical
Reg. No./Substance:
0/Activating Transcription Factor 2; 0/Cyclic AMP Response Element-Binding Protein; 0/DNA-Binding Proteins; 0/Fos-Related Antigen-2; 0/Myogenin; 0/Proto-Oncogene Proteins c-fos; 0/Proto-Oncogene Proteins c-jun; 0/RNA, Messenger; 0/Transcription Factor AP-1; 0/Transcription Factors

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


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