Literature DB >> 1656361

Jun inhibits myogenic differentiation.

H Y Su1, T J Bos, F S Monteclaro, P K Vogt.   

Abstract

Myoblasts from skeletal muscle of chicken or Japanese quail embryos were infected with avian sarcoma virus 17 (ASV-17), a retrovirus carrying the jun oncogene. At high multiplicities of infection ASV-17-induced morphologic transformation inhibited fusion of myoblasts into myotubes and stimulated extended replication. The expression of the muscle-specific proteins desmin, myosin and creatine phosphokinase was inhibited in ASV-17-infected cultures. Immunofluorescent staining detected strong expression of the ASV-17 Gag-Jun fusion protein in the nuclei of infected mononuclear myoblasts, but Gag-Jun was not detectable in multinucleated myotubes that occurred in clonal populations of ASV-17-infected quail myoblasts. This result suggests that the nuclear expression of viral jun and myogenic differentiation are mutually exclusive events. A mutant of ASV-17, ts jun-1, is partly temperature-sensitive in its ability to transform chicken embryo fibroblasts. At the non-permissive temperature of 41.5 degrees C, multinucleated myotubes readily formed in ts jun-1-infected myoblast cultures and expressed muscle-specific proteins detectable by immunofluorescent staining. These myotubes also showed strong immunofluorescent staining for Gag-Jun in the cell nuclei. The nuclear expression of a Jun protein that is defective in its transforming function appears therefore to be compatible with myogenesis. Several retroviral constructs carrying various viral and cellular jun inserts, as well as jun deletion mutants and recombinants between c-jun and v-jun, were tested for their effect on myogenic differentiation. There was an approximate correlation between the ability of a construct to transform chicken embryo fibroblasts and its effectiveness in interfering with myogenic differentiation. We conclude that the expression of an oncogenic jun gene in myoblasts strongly inhibits myogenic differentiation, and that a highly transforming Jun protein cannot be expressed in the nuclei of differentiating myotubes, while the presence of transformation-defective variants of Jun is compatible with differentiation.

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Mesh:

Year:  1991        PMID: 1656361

Source DB:  PubMed          Journal:  Oncogene        ISSN: 0950-9232            Impact factor:   9.867


  13 in total

1.  Sodium butyrate inhibits myogenesis by interfering with the transcriptional activation function of MyoD and myogenin.

Authors:  L A Johnston; S J Tapscott; H Eisen
Journal:  Mol Cell Biol       Date:  1992-11       Impact factor: 4.272

2.  Mutations in the Jun delta region suggest an inverse correlation between transformation and transcriptional activation.

Authors:  L S Håvarstein; I M Morgan; W Y Wong; P K Vogt
Journal:  Proc Natl Acad Sci U S A       Date:  1992-01-15       Impact factor: 11.205

3.  An essential role of phosphatidylinositol 3-kinase in myogenic differentiation.

Authors:  B H Jiang; J Z Zheng; P K Vogt
Journal:  Proc Natl Acad Sci U S A       Date:  1998-11-24       Impact factor: 11.205

4.  Tumor cell complementation groups based on myogenic potential: evidence for inactivation of loci required for basic helix-loop-helix protein activity.

Authors:  A N Gerber; S J Tapscott
Journal:  Mol Cell Biol       Date:  1996-07       Impact factor: 4.272

5.  v-jun cooperates with v-erbB to transform the thrombocytic/megakaryocytic lineage.

Authors:  M Garcia; J Samarut
Journal:  Proc Natl Acad Sci U S A       Date:  1993-10-01       Impact factor: 11.205

6.  Cell cycle-dependent variations in c-Jun and JunB phosphorylation: a role in the control of cyclin D1 expression.

Authors:  L Bakiri; D Lallemand; E Bossy-Wetzel; M Yaniv
Journal:  EMBO J       Date:  2000-05-02       Impact factor: 11.598

7.  Localization of myogenin, c-fos, c-jun, and muscle-specific gene mRNAs in regenerating rat skeletal muscle.

Authors:  K Kami; K Noguchi; E Senba
Journal:  Cell Tissue Res       Date:  1995-04       Impact factor: 5.249

8.  fos/jun repression of cardiac-specific transcription in quiescent and growth-stimulated myocytes is targeted at a tissue-specific cis element.

Authors:  K McBride; L Robitaille; S Tremblay; S Argentin; M Nemer
Journal:  Mol Cell Biol       Date:  1993-01       Impact factor: 4.272

9.  Epstein-Barr virus latent membrane protein 2A regulates c-Jun protein through extracellular signal-regulated kinase.

Authors:  Shao-Yin Chen; Jean Lu; Yin-Chu Shih; Ching-Hwa Tsai
Journal:  J Virol       Date:  2002-09       Impact factor: 5.103

10.  SPARC and thrombospondin genes are repressed by the c-jun oncogene in rat embryo fibroblasts.

Authors:  A Mettouchi; F Cabon; N Montreau; P Vernier; G Mercier; D Blangy; H Tricoire; P Vigier; B Binétruy
Journal:  EMBO J       Date:  1994-12-01       Impact factor: 11.598

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