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J Appl Physiol 84: 1083-1087, 1998;
8750-7587/98 $5.00
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Vol. 84, Issue 3, 1083-1087, March 1998

Nerve-responsive troponin I slow promoter does not respond to unloading

David S. Criswell1, Vanessa R. M. Hodgson2, Edna C. Hardeman2, and Frank W. Booth1

1 Department of Integrative Biology, Pharmacology, and Physiology, University of Texas Medical School, Houston, Texas 77030; and 2 Muscle Development Unit, The Children's Medical Research Institute, Wentworthville, New South Wales 2145, Australia

We examined the regulation of the troponin I slow (TnIs) promoter during skeletal muscle unloading-induced protein isoform transition, by using a transgenic mouse line harboring the -4,200 to +12 base pairs region of the human TnIs promoter. Eighteen female transgenic mice (~30 g body mass) were randomly divided into two groups: weight-bearing (WB) controls (n = 9) and hindlimb unloaded (HU; n = 9). The HU mice were tail suspended for 7 days. Body mass was unchanged in the WB group but was reduced (-6%; P < 0.05) after the HU treatment. Absolute soleus muscle mass (-25%) and soleus mass relative to body mass (-16%) were both lower (P < 0.05) in the HU group compared with the WB mice. Northern blot analyses indicate that 7 days of HU result in a 64% decrease (P < 0.05) in the abundance of endogenous TnIs mRNA (µg/mg muscle) in the mouse soleus. Furthermore, there is a trend for the abundance of the fast troponin I mRNA to be increased (+34%). Analysis of transgenic chloramphenicol acetyltransferase activity in the soleus muscle revealed no difference (P > 0.05) between WB and HU groups. We conclude that additional elements are necessary for the TnIs gene to respond to an unloading-induced, slow-to-fast isoform transition stimulus.

transgenic mice; skeletal muscle; hindlimb unloading

JAP 84(3):1083-1087
0161-7567/98 $5.00 Copyright © 1998 the American Physiological Society


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