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Am J Physiol Cell Physiol 282: C528-C537, 2002. First published October 24, 2001; doi:10.1152/ajpcell.00355.2001
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Vol. 282, Issue 3, C528-C537, March 2002

Transcriptional regulation of the type I myosin heavy chain promoter in inactive rat soleus

K. A. Huey1, R. R. Roy3, F. Haddad1, V. R. Edgerton2,3, and K. M. Baldwin1

1 Department of Physiology and Biophysics, University of California, Irvine, Irvine 92697; and 2 Department of Physiological Science, and 3 Brain Research Institute, University of California, Los Angeles, Los Angeles, California 90095-1761

Chronic muscle inactivity with spinal cord isolation (SI) decreases expression of slow type I myosin heavy chain (MHC) while increasing expression of the faster MHC isoforms, primarily IIx. The purpose of this study was to determine whether type I MHC downregulation in the soleus muscle of SI rats is regulated transcriptionally and to identify cis-acting elements or regions of the rat type I MHC gene promoter involved in this response. One week of SI significantly decreased in vivo activity of the -3500-, -408-, -299-, -215-, and -171-bp type I MHC promoters. The activity of all tested deletions of the type I MHC promoter, relative to the human skeletal alpha -actin promoter, were significantly reduced in the SI soleus, except activity of the -171-bp promoter, which increased. Mutation of the beta e3 element (-214/-190 bp) in the -215- and -408-bp promoters and deletion of this element (-171-bp promoter) attenuated type I downregulation with SI. Gel mobility shift assays demonstrated a decrease in transcription enhancer factor-1 binding to the beta e3 element with SI, despite an increase in total binding to this region. These results demonstrate that type I MHC downregulation with SI is transcriptionally regulated and suggest that interactions between transcription enhancer factor-1 and the beta e3 element are likely involved in this response.

beta e3 DNA regulatory element; transcription enhancer factor-1; spinal cord isolation; chronic muscle inactivity


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