Affiliation:
1. Hubert H. Humphrey Center for Experimental Medicine and Cancer Research, The Hebrew University-Hadassah Medical School, Jerusalem 91120, Israel, 1 and
2. Department of Pharmacology, Cornell University Medical College, New York, New York 100212
Abstract
ABSTRACT
The
Rex-1
(
Zfp-42
) gene, which encodes an acidic zinc finger protein, is expressed at high levels in embryonic stem (ES) and F9 teratocarcinoma cells. Prior analysis identified an octamer motif in the
Rex-1
promoter which is required for promoter activity in undifferentiated F9 cells and is involved in retinoic acid (RA)-associated reduction in expression. We show here that the Oct-3/4 transcription factor, but not Oct-1, can either activate or repress the
Rex-1
promoter, depending on the cellular environment.
Rex-1
repression is enhanced by E1A. The protein domain required for Oct-3/4 activation was mapped to amino acids 1 to 35, whereas the domain required for Oct-3/4 repression was mapped to amino acids 61 to 126, suggesting that the molecular mechanisms underlying transcriptional activation and repression differ. Like Oct-3/4, Oct-6 can also lower the expression of the
Rex-1
promoter via the octamer site, and the amino-terminal portion of Oct-6 mediates this repression. In addition to the octamer motif, a novel positive regulatory element, located immediately 5′ of the octamer motif, was identified in the
Rex-1
promoter. Mutations in this element greatly reduce
Rex-1
promoter activity in F9 cells. High levels of a binding protein(s), designated Rox-1, recognize this novel DNA element in F9 cells, and this binding activity is reduced following RA treatment. Taken together, these results indicate that the
Rex-1
promoter is regulated by specific octamer family members in early embryonic cells and that a novel element also contributes to
Rex-1
expression.
Publisher
American Society for Microbiology
Subject
Cell Biology,Molecular Biology
Cited by
219 articles.
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