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Mol Cell Biol, June 1998, p. 3633-3644, Vol. 18, No. 6
0270-7306/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.

The Position and Length of the Steroid-Dependent Hypersensitive Region in the Mouse Mammary Tumor Virus Long Terminal Repeat Are Invariant despite Multiple Nucleosome B Frames

Gilberto Fragoso,dagger William D. Pennie,Dagger Sam John,§ and Gordon L. Hager*

Laboratory of Receptor Biology and Gene Expression, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892-5055

Received 22 January 1998/Returned for modification 2 March 1998/Accepted 6 March 1998

Stimulation of the mouse mammary tumor virus with steroids results in the generation of a DNase I-hypersensitive region (HSR) spanning the hormone responsive element (HRE) in the long terminal repeat. Restriction enzymes were used to characterize the accessibility of various sites within the HSR of mouse mammary tumor virus long terminal repeat-reporter constructions in four different cell lines. The glucocorticoid-dependent HSR was found to span minimally 187 bases, a stretch of DNA longer than that associated with histones in the core particle. Although the 5'-most receptor binding site within the HRE is downstream of -190, hypersensitive sites were found further upstream to at least -295. The relationship in the accessibility between pairs of sites in the vicinity of the HSR was further examined in one cell line by a two-enzyme restriction access assay. In the uninduced state, the accessibilities at these sites were found to be independent of each other. In contrast, when stimulated with hormone, the accessibilities at these sites were observed to become linked. That is, once a distinct promoter was activated, all of the sites within the HSR of that molecule became accessible. The HSR formed along an invariant stretch of DNA sequence despite the multiplicity of nucleosome frames in the nucleosome B region, where the HRE is located. The results indicate that the macroscopic length of the HSR does not arise from core length-remodeling events in molecules containing Nuc-B in alternative positions.

* Corresponding author. Mailing address: Laboratory of Receptor Biology and Gene Expression, Bldg. 41, Rm. B602, National Cancer Institute, National Institutes of Health, 41 Library Dr., MSC 5055, Bethesda, MD 20892-5055. Phone: (301) 496-9867. Fax: (301) 496-4951. E-mail: hagerg{at}dce41.nci.nih.gov.

dagger Present address: Department of Biology, Johns Hopkins University, Baltimore, MD 21218.

Dagger Present address: Zeneca Laboratories, Macclesfield, United Kingdom.

§ Present address: Department of Biochemistry and Molecular Biology, Pennsylvania State University, University Park, PA 16802-4500.

Mol Cell Biol, June 1998, p. 3633-3644, Vol. 18, No. 6
0270-7306/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.


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