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J. Biol. Chem., Vol. 264, Issue 27, 15936-15942, 09, 1989
MA Magnuson and KD Shelton
An alternate promoter in the glucokinase gene is active in the beta cell
and produces a glucokinase mRNA which is longer and that has a different
leader sequence and translation start site than the hepatic glucokinase
mRNA. The glucokinase beta cell promoter is located at least 12 kilobases
upstream from the glucokinase hepatic promoter. Transcription from the
glucokinase beta cell promoter initiates over a region of 62 bases. The
absence of a TATA box homology in the proximal promoter region may account
for the diffuse transcriptional initiation. Translation of the beta cell
glucokinase mRNA predicts a glucokinase isozyme that is different from the
hepatic isozyme by 15 amino acids at the N terminus. The use of alternative
promoters apparently enables the glucokinase gene to be regulated by
insulin in the liver and by glucose in the beta cell, thus possibly
constituting an important feedback control loop for maintaining glucose
homeostasis. Alternate RNA splicing of the beta cell glucokinase mRNA
predicts at least two beta cell glucokinase isoforms. An alternate splice
acceptor site in the 4th exon of the glucokinase gene was identified in two
glucokinase cDNAs from rat insulinoma tissue. Use of the alternate splice
acceptor site results in a 51-nucleotide in frame deletion in the beta cell
glucokinase mRNA and removal of 17 amino acids from a region of the protein
situated between the putative glucose and ATP binding domains. Analysis of
the pattern of RNA splicing in tissues containing beta cells indicates that
the splice acceptor site utilized in producing hepatic glucokinase mRNA is
also utilized in the beta cell.
An alternate promoter in the glucokinase gene is active in the pancreatic beta cell
Department of Molecular Physiology and Biophysics, Vanderbilt University Medical School, Nashville, Tennessee 37232.
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