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Molecular and Cellular Biology, November 2006, p. 8607-8622, Vol. 26, No. 22
0270-7306/06/$08.00+0 doi:10.1128/MCB.00678-06
Copyright © 2006, American Society for Microbiology. All Rights Reserved.
Activation of Saccharomyces cerevisiae HIS3 Results in Gcn4p-Dependent, SWI/SNF-Dependent Mobilization of Nucleosomes over the Entire Gene
Yeonjung Kim,1,
Neil McLaughlin,1
Kim Lindstrom,2
Toshio Tsukiyama,2 and
David J. Clark1*
Laboratory
of Molecular Growth Regulation, National Institute of Child Health and
Human Development, National Institutes of Health, Building 6A, Room
2A14, 6 Center Drive, Bethesda, Maryland
20892,1
Division of Basic
Sciences, Fred Hutchinson Cancer Research Center, Seattle,
Washington 981092
Received 19 April 2006/
Returned for modification 30 May 2006/
Accepted 3 September 2006
The
effects of transcriptional activation on the chromatin structure of the
Saccharomyces cerevisiae HIS3 gene were
addressed by mapping the precise positions of nucleosomes in uninduced
and induced chromatin. In the absence of the Gcn4p activator,
the HIS3 gene is organized into a predominant nucleosomal
array. In wild-type chromatin, this array is disrupted, and several
alternative overlapping nucleosomal arrays are formed. The disruption
of the predominant array also requires the SWI/SNF remodeling machine,
indicating that the SWI/SNF complex plays an important role in
nucleosome mobilization over the entire HIS3 gene. The Isw1
remodeling complex plays a more subtle role in determining nucleosome
positions on HIS3, favoring positions different from those
preferred by the SWI/SNF complex. Both the SWI/SNF and Isw1 complexes
are constitutively present in HIS3 chromatin, although Isw1
tends to be excluded from the HIS3 promoter. Despite the
apparent disorder of HIS3 chromatin generated by the formation
of multiple nucleosomal arrays, nucleosome density profiles indicate
that some long-range order is always present. We propose that Gcn4p
stimulates nucleosome mobilization over the entire HIS3 gene
by the SWI/SNF complex. We suggest that the net effect of interplay
among remodeling machines at HIS3 is to create a highly
dynamic chromatin
structure.
* Corresponding
author. Mailing address: Laboratory of Molecular Growth Regulation,
National Institute of Child Health and Human Development, National
Institutes of Health, Building 6A, Room 2A14, 6 Center Drive, Bethesda,
MD 20892. Phone: (301) 496-6966. Fax: (301) 480-1907. E-mail:
clarkda{at}mail.nih.gov.
Published ahead of print on 18 September 2006.
Present
address: Division of Structural and Functional Genomics, Center for
Genome Science, National Institute of Health, KCDC, Seoul, South
Korea.
Molecular and Cellular Biology, November 2006, p. 8607-8622, Vol. 26, No. 22
0270-7306/06/$08.00+0 doi:10.1128/MCB.00678-06
Copyright © 2006, American Society for Microbiology. All Rights Reserved.
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