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Mol Cell Biol, February 1998, p. 1065-1073, Vol. 18, No. 2
0270-7306/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.

Epidermal Growth Factor Induction of the c-jun Promoter by a Rac Pathway

Nicole Clarke,1 Natalia Arenzana,1 Tsonwin Hai,2 Audrey Minden,1 and Ron Prywes1,*

Department of Biological Sciences, Columbia University, New York, New York 10027,1 and Ohio State Biochemistry Program and Department of Medical Biochemistry and Neurobiotechnology Center, Ohio State University, Columbus, Ohio 432102

Received 1 August 1997/Returned for modification 17 September 1997/Accepted 31 October 1997

The c-jun proto-oncogene encodes a transcription factor which is activated by mitogens both transcriptionally and by phosphorylation by Jun N-terminal kinase (JNK). We have investigated the cellular signalling pathways involved in epidermal growth factor (EGF) induction of the c-jun promoter. We find that two sequence elements, which bind ATF1 and MEF2D transcription factors, are required in HeLa cells, although they are not sufficient for maximal induction. Activated forms of Ras, RacI, Cdc42Hs, and MEKK increased expression of the c-jun promoter, while dominant negative forms of Ras, RacI, and MEK kinase (MEKK) inhibited EGF induction. These and previously published results suggest that EGF activates the c-jun promoter by a Ras-to-Rac-to-MEKK pathway. This pathway is similar to that used for posttranslational activation of c-jun by JNK.

* Corresponding author. Mailing address: Department of Biological Sciences, Columbia University, 1212 Amsterdam Ave. MC2420, New York, NY 10027. Phone: (212) 854-8281. Fax: (212) 865-8246. E-mail: mrp6{at}columbia.edu.




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