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Vol. 13, Issue 6, 1940-1952, June 2002
*Department of Biochemistry, Hong Kong University of Science and
Technology, Clear Water Bay, Kowloon, Hong Kong, People's Republic of
China; §School and Department of Medicine, University of
California, San Diego, La Jolla, California 92095;
In this report, we identify myogenin as an important
transcriptional target under the control of three intracellular
signaling pathways, namely, the p38 mitogen-activated protein
kinase- (MAPK), calcium-calmodulin-dependent protein kinase- (CaMK),
and calcineurin-mediated pathways, during skeletal muscle
differentiation. Three cis-elements (i.e., the E
box, myocyte enhancer factor [MEF] 2, and MEF3 sites) in the proximal
myogenin promoter in response to these three pathways are defined.
MyoD, MEF2s, and Six proteins, the trans-activators bound to these cis-elements, are shown to be activated
by these signaling pathways. Our data support a model in which all
three signaling pathways act in parallel but nonredundantly to control myogenin expression. Inhibition of any one pathway will result in
abolished or reduced myogenin expression and subsequent phenotypic differentiation. In addition, we demonstrate that CaMK and calcineurin fail to activate MEF2s in Rhabdomyosarcoma-derived RD cells. For CaMK,
we show its activation in response to differentiation signals and its
effect on the cytoplasmic translocation of histone deacetylases 5 are
not compromised in RD cells, suggesting histone deacetylases 5 cytoplasmic translocation is necessary but not sufficient, and additional signal is required in conjunction with CaMK to activate MEF2 proteins.
Department of Oncology, University of Western Ontario,
London, Ontario, Canada N6A 4L6; and ¶Molecular Oncology
Group, Department of Medicine, McGill University Health Center,
Montreal, Quebec, Canada H3A 1A1
These authors contributed equally to this work.
Present address: Division of Medical Oncology, Box
1128, Mount Sinai Medical Center, One Gustave L. Levy Place, New York, NY 10029.
#
Corresponding author. E-mail address:
bczgwu{at}ust.hk.
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