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Molecular and Cellular Biology, September 2000, p. 6668-6676, Vol. 20, No. 18
0270-7306/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.
Preferential Accessibility of the Yeast his3 Promoter
Is Determined by a General Property of the DNA Sequence, Not
by Specific Elements
Xuhong
Mai,
Susanna
Chou, and
Kevin
Struhl*
Department of Biological Chemistry and
Molecular Pharmacology, Harvard Medical School, Boston,
Massachusetts 02115
Received 13 April 2000/Returned for modification 29 May
2000/Accepted 7 June 2000
Yeast promoter regions are often more accessible to nuclear
proteins than are nonpromoter regions. As assayed by HinfI
endonuclease cleavage in living yeast cells, HinfI sites
located in the promoters of all seven genes tested were 5- to 20-fold
more accessible than sites in adjacent nonpromoter regions.
HinfI hypersensitivity within the his3 promoter
region is locally determined, since it was observed when this region
was translocated to the middle of the ade2 structural gene.
Detailed analysis of the his3 promoter indicated that
preferential accessibility is not determined by specific elements such
as the Gcn4 binding site, poly(dA-dT) sequences, TATA elements, or
initiator elements or by transcriptional activity. However, progressive
deletion of the promoter region in either direction resulted in a
progressive loss of HinfI accessibility. Preferential
accessibility is independent of the Swi-Snf chromatin remodeling
complex, Gcn5 histone acetylase complexes Ada and SAGA, and Rad6, which
ubiquitinates histone H2B. These results suggest that preferential
accessibility of the his3 (and presumably other) promoter
regions is determined by a general property of the DNA sequence (e.g.,
base composition or a related feature) rather than by defined sequence
elements. The organization of the compact yeast genome into inherently
distinct promoter and nonpromoter regions may ensure that transcription
factors bind preferentially to appropriate sites in promoters rather
than to the excess of irrelevant but equally high-affinity sites in
nonpromoter regions.
*
Corresponding author. Mailing address: Dept. of
Biological Chemistry and Molecular Pharmacology, Harvard
University, Boston, MA 02115. Phone: (617) 432-2104. Fax: (617)
432-2529. E-mail: kevin{at}hms.harvard.edu.
Molecular and Cellular Biology, September 2000, p. 6668-6676, Vol. 20, No. 18
0270-7306/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.
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