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J Biol Chem, Vol. 274, Issue 12, 8129-8136, March 19, 1999
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From the Departments of We have defined how four elements that regulate
expression of the rat skeletal muscle type 1 sodium channel (SkM1) gene
cooperate to yield specific expression in differentiated muscle. A
basal promoter region containing within it a promoter E-box ( Neuroscience,
¶ Neurology, and Biochemistry and Biophysics, University of
Pennsylvania School of Medicine, Philadelphia, Pennsylvania 19104
31/26) is broadly expressed in many cells, including myoblasts and myotubes; mutations within the promoter E-box that disrupt binding of the myogenic basic helix-loop-helix (bHLH) factors reduce expression in all
cell types only slightly. Sequential addition of upstream elements to the wild-type promoter confer increasing specificity of
expression in differentiated cells, even though all three
upstream elements, including a positive element (85/57),
a repressor E-box (90/85), and upstream repressor sequences
(135/95), bind ubiquitously expressed transcription factors.
Mutations in the promoter E-box that disrupt the binding of the bHLH
factors counteract the specificity conferred by addition of the
upstream elements, with the greatest interaction observed between the
upstream repressor sequences and the promoter E-box. Forced expression of myogenin in myoblasts releases repression exerted by the upstream repressor sequences in conjunction with the wild-type, but not mutant,
promoter E-box, and also initiates expression of the endogenous SkM1
protein. Our data suggest that particular myogenic bHLH proteins bound
at the promoter E-box control expression of SkM1 by releasing repression exerted by upstream repressor sequences in differentiated muscle cells.
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