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Journal of Lipid Research, Vol 36, 1507-1521, Copyright © 1995 by Lipid Research, Inc.
CF Semenkovich, T Coleman and FT Fiedorek Jr
To better understand the accelerated decay of fatty acid synthase (FAS)
message that occurs after glucose deprivation (J. Biol. Chem. 1993. 268:
6961-6970), we characterized the 3' terminus of the human message and the
kinetics of FAS mRNA decay in HepG2 cells. The FAS gene was localized to
human chromosome 17q24-25 and to syntenic distal mouse chromosome 11.
Expression of the FAS message in human tissues was ubiquitous with high
levels in liver, lung, and intra-abdominal adipose tissue. The 806
nucleotide 3' untranslated region of the human mRNA contained two regions
with the instability pentamer AUUUA. Unlike short- lived messages
containing AUUUA motifs, FAS mRNA decay after glucose deprivation was not
first order, and there were no detectable changes in the poly(A) tail.
Glucose deprivation transiently caused FAS message to sediment more rapidly
than control message in density gradients. In vivo treatment with different
translational inhibitors showed that translation per se was not necessary
for FAS mRNA decay; association of polysomes with FAS message protected it
from decay. In cell-free decay experiments, FAS mRNA decay was more rapid
using components from glucose-deprived than glucose-treated cells. These
data suggest that glucose regulates cytoplasmic HepG2 FAS mRNA stability by
partitioning the message between a translated pool not subject to
degradation and a decay compartment, features reminiscent of regulated
stability for other diet-responsive messages.
ARTICLES
Human fatty acid synthase mRNA: tissue distribution, genetic mapping, and kinetics of decay after glucose deprivation
Department of Medicine, Washington University School of Medicine, St. Louis, MO 63110, USA.
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