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J Biol Chem, Vol. 274, Issue 4, 2372-2378, January 22, 1999
From the Departments of An element required for glucocorticoid repression
of mouse gonadotropin-releasing hormone (GnRH) gene transcription, the
distal negative glucocorticoid response element (nGRE), is not bound directly by glucocorticoid receptors (GRs) but is recognized by Oct-1
present in GT1-7 cell nuclear extracts or by Oct-1 purified from HeLa
cells. Furthermore, purified full-length GRs interact directly with
purified Oct-1 bound to the distal nGRE. Increasing the extent of
distal nGRE match to an Oct-1 consensus site not only increases the
affinity of Oct-1 binding, but also alters the conformation of
DNA-bound Oct-1 and the pattern of protein DNA complexes formed
in vitro with GT1-7 cell nuclear extracts. In addition,
the interaction of purified GR with DNA-bound Oct-1 is altered when
Oct-1 is bound to the consensus Oct-1 site. Mutation of the distal nGRE
to a consensus Oct-1 site is also associated with reduced
glucocorticoid repression in transfected GT1-7 cells. Furthermore,
repression of GnRH gene transcription by
12-O-tetradecanoylphorbol-13-acetate, which utilizes
sequences that overlap with the nGRE, is reversed by this distal nGRE
mutation leading to activation of GnRH gene transcription. Thus,
changes in the assembly of multi-protein complexes at the distal nGRE
can influence the regulation of GnRH gene transcription.
The Glucocorticoid Receptor Is Tethered to DNA-bound Oct-1 at
the Mouse Gonadotropin-releasing Hormone Distal Negative Glucocorticoid
Response Element
,¶
Biological Sciences,
¶ Neuroscience, and Pharmacology, University of Pittsburgh,
Pittsburgh, Pennsylvania 15260 and the § Laboratory of
Receptor Biology and Gene Expression, NCI, National Institutes of
Health, Bethesda, Maryland 20892-5055
Copyright © 1999 by The American Society for Biochemistry and Molecular Biology, Inc.
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