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J Biol Chem, Vol. 275, Issue 2, 1398-1404, January 14, 2000
From the Department of Molecular Genetics, Biochemistry, and
Microbiology, University of Cincinnati College of Medicine,
Cincinnati, Ohio 45267-0524
Using a Drosophila transgenic system
we investigated the ability of GAGA factor, a putative anti-repressor,
to modulate transcription-related events in the absence or presence of
a bona fide activator, the Adf-1 transcription factor. In
contrast to previous in vitro and in vivo data
linking the binding of GAGA factor to the acquisition of DNase
hypersensitivity at heat shock promoters, we observed that inserting
multiple GAGA binding motifs adjacent to a minimal alcohol
dehydrogenase (Adh) promoter led to strongly elevated embryonic transcription without creation of a promoter-associated DNase-hypersensitive (DH) site. Establishment of DNase hypersensitivity required the presence of both GAGA and Adf-1 binding sites and was
accompanied by a further, synergistic increase in transcription. Because Adf-1 is capable neither of establishing a DH site nor of
promoting efficient transcription by itself in embryos, it is likely
that DH site formation depends on a GAGA factor-mediated binding of
Adf-1 to chromatin, perhaps facilitated by a locally remodeled
downstream promoter region. More generally we suggest that GAGA
factor-binding sequences may operate in a promoter-specific context,
with transcriptional activation, polymerase pausing, and/or DH site
formation critically dependent on the nature of the sequences (and
their binding partners) linked in cis.
GAGA Factor-dependent Transcription and Establishment
of DNase Hypersensitivity Are Independent and Unrelated Events in
Vivo*
and
*
This work was supported in part by NIEHS, National
Institutes of Health Grant P30-ES06096.The costs of publication of this article were defrayed in part by the
payment of page charges. The article
must therefore be hereby marked
"advertisement" in accordance with 18 U.S.C. Section
1734 solely to indicate this fact.
Recipient of an Albert J. Ryan Fellowship. Partially supported by
NCI, National Institutes of Health Grant T32-CA59268. Present address:
Cell Biology and Metabolism Branch, NICHD, NIH, Bethesda, MD 20892.
§
To whom correspondence should be addressed: Dept. of Molecular
Genetics, Biochemistry, and Microbiology, University of Cincinnati College of Medicine, 231 Bethesda Ave., Cincinnati, OH 45267-0524. Tel.: 513-558-5532; Fax: 513-558-8474; E-mail:
cartwril@ucmail.uc.edu.
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