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Laboratory of Molecular Endocrinology, Massachusetts General Hospital, Howard Hughes Medical Institute, Harvard Medical School Boston, Massachusetts 02114
Address requests for reprints to: Dr. Joel F. Habener, Laboratory of Molecular Endocrinology, Massachusetts General Hospital, Howard Hughes Medical Institute, Harvard Medical, School, Boston, Massachusetts 02114.
Abstract
The rat glucagon gene 5'-flanking region contains a pancreatic islet-specific enhancer-like element, G3. It has been shown previously that G3-binding and transactivating proteins are present in islet cell lines expressing the glucagon, somatostatin, and insulin genes, but not in several nonislet cell lines. The present study now shows that the glucagon G3 transcription factor binds to DNA sequences within cis-acting elements of the rat somatostatin and rat insulin-I genes that have been defined by others as pancreatic islet-specific transcriptional enhancers. In addition, when fused to glucagon or somatostatin minimal promoters in reporter plasmids, these enhancer elements of the three islet hormone-producing genes functionally activate transcription when transfected into islet cell lines producing glucagon, insulin, or somatostatin. The enhancer elements of the three different islet polypeptide hormone genes define a potential consensus motif that binds islet cell type-specific transcription factors.
FOOTNOTES
This work was supported in part by USPHS Grants DK-30834 and DK-30457.
* Present address: Department of Biochemical Pharmacology, Center for Pharmacology and Toxicology, University of Goettingen, D3400 Goettingen, Germany. Supported by theDeutsche Forschungsgemeinschaft (Bonn, Germany).
Received for publication February 20, 1991. Revision received July 12, 1991. Accepted for publication July 12, 1991.
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