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Volume 271, Number 36, Issue of September 6, 1996 pp. 22231-22239
©1996 by The American Society for Biochemistry and Molecular Biology, Inc.

The Initiator Element and Proximal Upstream Sequences Affect Transcriptional Activity and Start Site Selection in the Amyloid beta -Protein Precursor Promoter

(Received for publication, April 30, 1996, and in revised form, July 5, 1996)

Wolfgang W. Quitschke , James P. Matthews , Richard J. Kraus § and Alexander A. Vostrov

From the Department of Psychiatry and Behavioral Science, State University of New York at Stony Brook, Stony Brook, New York 11794-8101 and the § McArdle Laboratory for Cancer Research, University of Wisconsin Medical School, Madison, Wisconsin 53706-1599

The TATA-less human amyloid beta -protein precursor promoter contains an initiator element with the sequence CGTCA+1GTT. Primary transcriptional start sites were identified at positions +1 and -4. Deletion of the upstream activator elements APBbeta and APBalpha did not affect the selection of transcriptional start sites, although total transcriptional activity was reduced both in vitro and in vivo. Mutations within the initiator element shifted the transcriptional start sites and reduced transcriptional activity. Mutations between positions -6 and -35 changed the relative utilization of start sites +1 and -4 without affecting the total level of transcriptional activity. A 10-base pair deletion between position -40 and -31 increased in vitro transcriptional activity with a preeminent utilization of the start site at position -4. In contrast, a 20-base pair deletion between position -40 and -21 resulted in a reduction in transcriptional activity and in the primary utilization of the start site at position +1. Furthermore, transactivation by APBbeta and APBalpha was eliminated. DNase I footprinting provided evidence for the existence of two binding domains designated UE (position -12 to -30) and Inr (position +7 to -7). The positions of these binding domains are altered in mutations and deletions that affect transcriptional activity.


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