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J. Biol. Chem., Vol. 276, Issue 47, 43524-43533, November 23, 2001
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From the Department of Molecular, Cellular, and Developmental
Biology, University of Colorado, Boulder, Colorado 80309-0347
Mammalian skeletal muscles are a mosaic of
different fiber types largely defined by differential myosin heavy
chain (MyHC) expression. Little is known about the molecular mechanisms
regulating expression of the MyHC gene family members in different
fiber types. In this work, we identified several cis- and
trans-elements that regulate expression of the three adult
fast MyHC genes. Despite multiple DNA-binding motifs for well
characterized muscle transcription factors upstream of all three fast
MyHC genes, expression of MyoD/Myf-5, calcineurin, or NFAT3 had
different effects on the three promoters. MyoD or Myf-5 overexpression
preferentially activated the IIb promoter, whereas NFAT or activated
calcineurin overexpression preferentially activated the IIa promoter.
Calcineurin had a 50-100-fold stimulatory effect on the IIa promoter,
and the known downstream effectors of calcineurin (myocyte enhancer
factor-2 and NFAT) cannot completely account for this activation.
Finally, we identified two elements critical for regulating MyHC-IId/x
expression: a 130-base pair enhancer element and a CArG-like element
that inhibited IId/x promoter activity in vitro. Thus, we
have found specific regulatory pathways that are distinct for the three
adult fast MyHC genes. These elements are logical candidates for
fiber-specific control of skeletal muscle gene expression in
vivo.
The nucleotide sequence(s) reported in this paper has been submitted to the GenBankTM/EMBL Data Bank with accession number(s) AF081358 and AF081359.
Different Pathways Regulate Expression of the Skeletal Myosin
Heavy Chain Genes*
, and
*
This work was supported in part by National Institutes of
Health Grants RO1-GM29090 (to L. A. L.) and F32AR08443 (to
C. A. S.) and by a Muscular Dystrophy Association research
fellowship grant (to D. L. A.).The costs of publication of this
article were defrayed in part by the
payment of page charges. The article
must therefore be hereby marked
"advertisement" in
accordance with 18 U.S.C. Section
1734 solely to indicate this fact.
Supported by the Undergraduate Research Opportunities Program of
the University of Colorado (Boulder, CO).
§
To whom correspondence should be addressed: Dept. of Molecular,
Cellular, and Developmental Biology, University of Colorado, Campus Box
347, Boulder, CO 80309-0347. Tel.: 303-492-7606; Fax: 303-492-8907;
E-mail: leinwand@stripe.colorado.edu.
Copyright © 2001 by The American Society for Biochemistry and Molecular Biology, Inc.
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