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Molecular and Cellular Biology, March 2004, p. 2444-2454, Vol. 24, No. 6
0270-7306/04/$08.00+0     DOI: 10.1128/MCB.24.6.2444-2454.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.

Elongation Inhibition by DRB Sensitivity-Inducing Factor Is Regulated by the A20 Promoter via a Novel Negative Element and NF-B

Department of Biological Chemistry, The Weizmann Institute of Science, Rehovot 76100, Israel,¹ Department of Biological Information, Tokyo Institute of Technology,² PRESTO, Japan Science and Technology Corporation, 4259 Nagatsuta, Yokohama 226-8501, Japan³

Received 9 June 2003/ Returned for modification 25 September 2003/ Accepted 18 December 2003

A20 is an immediate-early NF-B target gene. Prior to NF-B stimulation, the A20 promoter is bound by the polymerase II machinery to allow rapid transcription activation. Here we show that the basal A20 transcription is repressed at the level of elongation in a promoter-specific fashion. Immunodepletion in vitro and RNA interference in cultured cells suggest that the basal elongation inhibition is conferred by DRB sensitivity-inducing factor (DSIF). We have identified a negative upstream promoter element called ELIE that controls DSIF activity. Remarkably, following NF-B stimulation, inhibition of the A20 promoter by DSIF persists, but it is now regulated by NF-B rather than ELIE. Similar regulation by DSIF is shown for another NF-B-responsive gene, the IB gene. These findings reveal an intimate and dynamic relationship between DSIF inhibition of elongation and promoter-bound transcription factors. The potential significance of the differential regulation of DSIF activity by cis-acting elements is discussed.

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