Overexpression of myotonic dystrophy kinase in BC3H1 cells induces the skeletal muscle phenotype.
Myotonic muscular dystrophy is an autosomal dominant defect that produces muscle wasting, myotonia, and cardiac conduction abnormalities. The myotonic dystrophy locus codes for a putative serine-threonine protein kinase of unknown function. We report that overexpression of human myotonic dystrophy protein kinase induces the expression of skeletal muscle-specific genes in undifferentiated BC3H1 muscle cells. BC3H1 clones expressing myotonic dystrophy kinase appear equivalent to differentiated cells with respect to expression of myogenin, retinoblastoma tumor supressor gene, M creatine kinase, beta-tropomyosin, and vimentin. In addition, differential display analysis demonstrates that the pattern of gene expression exhibited by myotonic dystrophy kinase-expressing cells is essentially identical to that of differentiated BC3H1 muscle cells. These observations suggest that myotonic dystrophy kinase may function in the myogenic pathway.
Department of Medicine, University of Colorado Health Sciences Center, Denver 80262, USA.
E W
EW
Bush
C S
CS
Taft
G E
GE
Meixell
M B
MB
Perryman
D001483:Base Sequence; D002460:Cell Line; D003402:Creatine Kinase / Q000235:genetics / Q000378:metabolism; D018076:DNA, Complementary; D015971:Gene Expression Regulation, Enzymologic; D006801:Humans; D007527:Isoenzymes; D008969:Molecular Sequence Data; D018482:Muscle, Skeletal / Q000201:enzymology*; D009223:Myotonic Dystrophy / Q000201:enzymology*; D010641:Phenotype; D017346:Protein Serine-Threonine Kinases / Q000235:genetics* / Q000378:metabolism; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism
D018076:DNA, Complementary; D007527:Isoenzymes; D012333:RNA, Messenger; D017346:Protein Serine-Threonine Kinases; D003402:Creatine Kinase