In this report we demonstrate that approximately 1.1 kb of the rat glu
cagon gene promoter upstream of the transcriptional start site specifi
cally directs the transcription of the reporter gene chloramphenicol a
cetyl transferase (CAT) (p[-1.1]GLU-CAT) in insulinoma beta-TC1 cells.
On the contrary, the 350 bp closest to the transcription start site (
p[-0.35]GLU-CAT) are ineffective in beta-TC1 cells. Both constructs ar
e transcriptionally active in InR1-G9 glucagonoma cells. While protein
kinase A and protein kinase C activators, acting through independent
pathways, strongly increase both the transcription of p[-1.1]GLU-CAT a
nd the accumulation of glucagon transcript in beta-TC1 cells, they are
weaker activators in InR1-G9 cells. Our experiments suggest that some
positive transcription control elements, necessary for the glucagon g
ene transcription in insulinoma beta-TC1 cells, are localized in the -
350/-1100 region of the glucagon gene. Furthermore, our data indicate
that glucagon gene transcription can be strongly activated through the
protein kinase A pathway in some specific cellular contexts. (C) 1995
Academic Press, Inc.