Srf and tef-1 control of chicken skeletal _-actin gene during slow
-muscle hypertrophy.
Carson, James A., Robert J. Schwartz, and Frank W. Booth.
Department of Integrative Biology, University of Texas-Houston
Health Science Center, 6431 Fannin, 4.100 MSB, Houston, TX 77030,
Department of Cell Biology, Baylor College of Medicine, One Baylor
Plaza, Houston, TX 77030
APStracts 2:0430C, 1995.
The purpose of this study was to delineate the [alpha]-actin
regulatory elements and transcription factors that are responsible
for conferring stretch overload responsiveness during hypertrophy of
the anterior latissimus dorsi (ALD) muscle of young chickens by
weighting one wing. Minimal promoter constructs were evaluated by
direct injection into the ALD which demonstrated that both SRE1 and
the TEF-1 elements were sufficient for increased expression during
stretch overload. A mutated SRE1 prevented expression in both basal
and stretched ALD muscles, while a mutated TEF-1 element reduced
actin promoter function in both control and stretched muscles. The
SRF-SRE1 binding complex demonstrated faster migration in mobility
shift assays from day 3 and day 6 stretched ALD nuclear extracts,
relative to their control. TEF-1 binding was qualitatively increased
in stretched extracts at day 3, but not day 6 of stretch overload.
Skeletal [alpha]-actin mRNA accumulated from day 3 to day 6 of
stretch overload. These data demonstrate that SRE1 is necessary and
sufficient for stretch-overload responsiveness from the skeletal
[alpha]-actin promoter and that the SRF-SRE1 binding complex migrates
faster in stretched nuclear extracts of hypertrophied relative to
control extracts from intact ALD muscles of chickens.
Received 7 August 1995; accepted in final form 20 November 1995.
APS Manuscript Number C485-5.
Article publication pending Am. J. Physiol. (Cell Physiology).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 8 December 95