Nucleic Acids Research, 1991, Vol. 19, No. 7 1585-1591
© 1991
MOLECULAR BIOLOGY |
Transcriptional control of c-jun by retinoic acid
Hubrecht Laboratory, Netherlands Institute for Developmental Biology Uppsalalaan 8, 3584 CT Utrecht, The Netherlands
* To whom correspondence should be addressed
Received December 5, 1990. Revised March 4, 1991. Accepted March 4, 1991.
The proto-oncogene c-jun, a major component of transcription factor AP-1, is expressed at very low levels in undifferentiated embryonal carcinoma (EC) end embryonic stem (ES) cells. Retinoic acid (RA) induced differentiation causes a strong increase in the levels of c-jun mRNA. In this paper we report the cloning and characterization of the mouse c-jun promoter. Our results show that RA treatment causes a strong enhancement in c-jun promoter activity, an effect probably mediated by the RA-receptor ß (RARß). Sequences located between –329 and –293 are responsible for the observed RA effect, and bind at least five different protein complexes, of which three are decreased upon RA treatment. These protein binding sites do not resemble RA-responsive elements (RARE's) found in the promoters of retinoic acid receptor ß (RARß) and laminin B1. Furthermore, we could not detect a direct interaction of RAR
and RARß to these sequences, indicating that RA-induced c-jun expression is an indirect effect of RAR action.
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