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Articles in PresS, published online ahead of print October 22, 2001
Am J Physiol Cell Physiol, 10.1152/ajpcell.00355.2001
Submitted on July 27, 2001
Accepted on October 11, 2001
1 Physiology and Biophysics, University of California, Irvine, Irvine, CA, USA
2 Brain Research Institute, University of California, Los Angeles, Los Angeles, CA, USA
3 Physiological Sciences, University of California, Los Angeles, Los Angeles, CA, USA; Brain Research Institute, University of California, Los Angeles, Los Angeles, CA, USA
* To whom correspondence should be addressed. E-mail: kimberly.huey{at}asu.edu.
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 if rat type I MHC gene down-regulation in the soleus of SI rats is regulated transcriptionally and to identify cis elements or regions of the type I MHC promoter involved in this response. One week of SI significantly decreased in vivo activity of the -3500, -408, -299, -215, and -171 type I MHC promoters. The activity of all tested deletions of the type I MHC promoter, relative to the human 
skeletal actin promoter, were significantly reduced in the SI soleus except for activity of -171 promoter which increased. Mutation of the ße3 element (-214/-190) in both the -215 and -408 promoters and deletion of this element (-171 promoter) attenuated type I down-regulation with SI. Gel mobility shift assays demonstrated a decrease in transcription enhancer factor 1 (TEF-1) binding to the ße3 element with SI despite an increase in total binding to this region. These results demonstrate that type I MHC down-regulation with SI is transcriptionally regulated and suggest that interactions between TEF-1 and the ße3 element are likely involved in this response.
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