Regulation of the skeletal [alpha]-actin promoter in young chickens during
hypertrophy caused by stretch overload.
Carson, James A., Zhen Yan, Frank W. Booth, Michael E. Coleman, Robert J.
Schwartz, and Craig S. Stump.
Department of Physiology and Cell Biology, University of Texas-Houston
Health Science Center, Houston, Texas 77030; and Department of Cell Biology,
Baylor College of Medicine, Houston, Texas 77030
APStracts 2:0017C, 1995.
Anterior latissimus dorsi (ALD) muscles of three-week old male chickens were
injected with plasmids containing various lengths of the chicken skeletal
[alpha]-actin promoter (ranging _2090 to _77 relative to the transcription
start site) driving luciferase. Hypertrophy of the left ALD muscle was induced
by attaching a weight (11% of body weight) to the left wing of each chicken,
while the unweighted contralateral wing served as the control. Six days of
stretch overload significantly increased muscle mass 110%. Luciferase
activity from the -2090 actin-luciferase chimeric gene increased 127%, as
compared to the contralateral control ALD muscle. Luciferase activities
driven by the _424, _202, and _99 actin promoters were 179%, 134%, and 378%
higher, respectively, in the stretched ALD muscle than in the contralateral,
control ALD muscle. Luciferase activity from the _77 deletion construct was
not different between stretched and control muscles. These data indicate that
the gene region responding to stretch is downstream of _99 and imply, but do
not conclusively prove, that the region between _99 and _77, which contains
SRE1, contributes to the stretch-induced increase in skeletal [alpha]-actin
promoter activity in the ALD muscle.
Received 28 June 1994; accepted in final form 20 October 1994
APS Manuscript Number C368-4.
Article publication pending Am. J. Physiol. (Cell Physiology).
ISSN 1080-4757 Copyright 1994 The American Physiological Society.
Published in APStracts on 27 February 1995.