Mutation of MyoD-Ser237 abolishes its up-regulation by c-Mos

Recently we have shown that Mos could activate myogenic differentiation by promoting heterodimerisation of MyoD and E12 proteins. Here, we demonstrate that MyoD can be efficiently phosphorylated by in vitro kinase assay with purified Mos immunoprecipitated from transfected cells. Comparative two-dim...

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Bibliographic Details
Published in:FEBS letters 2000-06, Vol.474 (2), p.233-237
Main Authors: Pelpel, Karine, Leibovitch, Marie-Pierre, Fernandez, Anne, Leibovitch, Serge A.
Format: Article
Language:English
Subjects:
Amino Acid Substitution - genetics
Animals
c-Mos
Cell Line
Conserved Sequence - genetics
Creatine Kinase - genetics
Fibroblasts
Mice
Mutation - genetics
MyoD
MyoD Protein - chemistry
MyoD Protein - genetics
MyoD Protein - metabolism
Myogenesis
Organ Specificity
Peptide Fragments - chemistry
Peptide Fragments - metabolism
Peptide Mapping
Phosphorylation
Phosphoserine - metabolism
Promoter Regions, Genetic - genetics
Proto-Oncogene Proteins c-mos - genetics
Proto-Oncogene Proteins c-mos - metabolism
Recombinant Proteins - chemistry
Recombinant Proteins - genetics
Recombinant Proteins - metabolism
Serine - genetics
Serine - metabolism
Transcriptional Activation
Transfection
Trypsin - metabolism
Up-Regulation
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Summary:Recently we have shown that Mos could activate myogenic differentiation by promoting heterodimerisation of MyoD and E12 proteins. Here, we demonstrate that MyoD can be efficiently phosphorylated by in vitro kinase assay with purified Mos immunoprecipitated from transfected cells. Comparative two-dimensional tryptic phosphopeptide mapping combined with site-directed mutagenesis revealed that Mos phosphorylates MyoD on serine 237. Mutation of serine 237 to a non-phosphorylable alanine (MyoD-Ala237) abolished the positive regulation of MyoD by Mos following overexpression in proliferating 10T1/2 cells. Taken together, our data show that direct phosphorylation of MyoD-Ser237 by Mos plays a positive role in increasing MyoD activity during myoblast proliferation.
ISSN:0014-5793
1873-3468
DOI:10.1016/S0014-5793(00)01610-0