Key result
The human MyHC-IIb promoter exhibited significantly reduced transcriptional activity compared to the mouse sequence due to diminished MEF2 and SRF binding, although its mRNA expression was significantly up-regulated in Duchenne muscular dystrophy.
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Animal models leave open MyHC-IIb regulation in human muscle; human studies needed before clinical translation.
BACKGROUND: While the myosin heavy chain IIb isoform (MyHC-IIb) is the predominant motor protein in most skeletal muscles of rats and mice, the messenger RNA (mRNA) for this isoform is only expressed in a very small subset of specialized muscles in adult large mammals, including humans. RESULTS: We identify the DNA sequences limiting MyHC-IIb expression in humans and explore the activation of this gene in human skeletal muscle. We demonstrate that the transcriptional activity of ~1.0 kb of the human MyHC-IIb promoter is greatly reduced compared to that of the corresponding mouse sequence in both mouse and human myotubes in vitro and show that nucleotide differences that eliminate binding sites for myocyte enhancer factor 2 (MEF2) and serum response factor (SRF) account for this difference. Despite these differences, we show that MyHC-IIb mRNA is expressed in fetal human muscle cells and that MyHC-IIb mRNA is significantly up-regulated in the skeletal muscle of Duchene muscular dystrophy patients. CONCLUSIONS: These data identify the genetic basis for a key phenotypic difference between the muscles of large and small mammals, and demonstrate that mRNA expression of the MyHC-IIb gene can be re-activated in human limb muscle undergoing profound degeneration/regeneration.
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Harrison et al. (2011) studied Duchenne Muscular Dystrophy (n=20). Human MyHC-IIb promoter sequence vs. Mouse MyHC-IIb promoter sequence was evaluated on Transcriptional activity of the 1.0 kb MyHC-IIb promoter (p=<0.01). The human MyHC-IIb promoter exhibited significantly reduced transcriptional activity compared to the mouse sequence due to diminished MEF2 and SRF binding, although its mRNA expression was significantly up-regulated in Duchenne muscular dystrophy.
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