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Molecular and Cellular Biology, July 1999, p. 4711-4718, Vol. 19, No. 7
0270-7306/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.

Major Egr3 Isoforms Are Generated via Alternate Translation Start Sites and Differ in Their Abilities To Activate Transcription

Kevin J. O'Donovan and Jay M. Baraban*

Departments of Neuroscience and Psychiatry and Behavioral Sciences, Johns Hopkins University School of Medicine, Baltimore, Maryland

Received 9 December 1998/Returned for modification 10 February 1999/Accepted 6 April 1999

In previous studies, we detected a major, unidentified Egr response element (ERE) binding complex in brain extracts. We now report that this complex contains a truncated isoform of Egr3 generated by use of an alternate translation start site at methionine 106. Furthermore, the ERE binding complex previously thought to contain full-length Egr3 includes several isoforms generated by initiation at other internal methionines. Full-length and truncated (missing residues 1 to 105) Egr3 isoforms differ in the ability to stimulate transcription directed by a tandem repeat of two EREs but not by a single ERE. Taken together, our results indicate that alternative translation start sites are used to generate Egr3 isoforms with distinct transcriptional properties.

* Corresponding author. Mailing address: Department of Neuroscience, WBSB 908, Johns Hopkins University School of Medicine, 725 N. Wolfe St., Baltimore, MD 21205. Phone: (410) 955-2500. Fax: (410) 614-6249. E-mail: jbaraban{at}jhmi.edu.

Molecular and Cellular Biology, July 1999, p. 4711-4718, Vol. 19, No. 7
0270-7306/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.


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