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Submitted on August 10, 2001
Accepted on March 5, 2003
1 James R. Lambert Department of Pathology University of Colorado Health Sciences Center Denver, CO 80262 Tel: 303-315-8248
* To whom correspondence should be addressed. E-mail: steve.nordeen{at}uchsc.edu.
We have analyzed histone acetylation at the steroid-responsive mouse mammary tumor virus (MMTV) promoter in five separate cell lines that express functional glucocorticoid and/or progesterone receptors. Chromatin immunoprecipitation assays reveal that glucocorticoid and progesterone receptors bind the MMTV promoter after hormone addition but that receptor binding is not associated with an increase in acetylation of histone H3 or H4. We have, however, found one exception to this rule. Previously we described a cell line (T47D(C&L)) that displayed a remarkable differential induction of MMTV by glucocorticoids and progestins. At one chromosomal locus (MMTV-luciferase), MMTV is preferentially induced by glucocorticoids while at another locus within the same cell (MMTV-CAT), MMTV is activated by both glucocorticoids and progestins. Here we show that the glucocorticoid-mediated induction of MMTV-luciferase is accompanied by increased recruitment of CREB binding protein (CBP) to the promoter and increased histone H3 and H4 acetylation while the hormonal induction of MMTV-CAT in the same cell exhibit s a more modest CBP recruitment without any increase in histone acetylation. These studies suggest that increased histone acetylation may serve a potentiating function for MMTV activation at certain loci. However, increased histone acetylation is not requisite for steroid-mediated induction of transcription at all genes.
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