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Molecular and Cellular Biology, October 2001, p. 6450-6460, Vol. 21, No. 19
0270-7306/01/$04.00+0   DOI: 10.1128/MCB.21.19.6450-6460.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.

Widespread Collaboration of Isw2 and Sin3-Rpd3 Chromatin Remodeling Complexes in Transcriptional Repression

Thomas G. Fazzio,1,2 Charles Kooperberg,3 Jesse P. Goldmark,1 Cassandra Neal,4 Ryan Basom,4 Jeffrey Delrow,4 and Toshio Tsukiyama1,*

Division of Basic Sciences,1 Division of Public Health Sciences,3 and DNA Array Facility,4 Fred Hutchinson Cancer Research Center, Seattle, Washington 98109-1024, and Molecular and Cellular Biology Program, Fred Hutchinson Cancer Research Center and University of Washington, Seattle, Washington 981952

Received 9 May 2001/Returned for modification 19 June 2001/Accepted 27 June 2001

The yeast Isw2 chromatin remodeling complex functions in parallel with the Sin3-Rpd3 histone deacetylase complex to repress early meiotic genes upon recruitment by Ume6p. For many of these genes, the effect of an isw2 mutation is partially masked by a functional Sin3-Rpd3 complex. To identify the full range of genes repressed or activated by these factors and uncover hidden targets of Isw2-dependent regulation, we performed full genome expression analyses using cDNA microarrays. We find that the Isw2 complex functions mainly in repression of transcription in a parallel pathway with the Sin3-Rpd3 complex. In addition to Ume6 target genes, we find that many Ume6-independent genes are derepressed in mutants lacking functional Isw2 and Sin3-Rpd3 complexes. Conversely, we find that ume6 mutants, but not isw2 sin3 or isw2 rpd3 double mutants, have reduced fidelity of mitotic chromosome segregation, suggesting that one or more functions of Ume6p are independent of Sin3-Rpd3 and Isw2 complexes. Chromatin structure analyses of two nonmeiotic genes reveals increased DNase I sensitivity within their regulatory regions in an isw2 mutant, as seen previously for one meiotic locus. These data suggest that the Isw2 complex functions at Ume6-dependent and -independent loci to create DNase I-inaccessible chromatin structure by regulating the positioning or placement of nucleosomes.

* Corresponding author. Mailing address: Division of Basic Sciences, Fred Hutchinson Cancer Research Center, Mail Stop A1-162, 1100 Fairview Ave. North, Seattle, WA 98109-1024. Phone: (206) 667-4996. Fax: (206) 667-6497. E-mail: ttsukiya{at}fhcrc.org.

Molecular and Cellular Biology, October 2001, p. 6450-6460, Vol. 21, No. 19
0270-7306/01/$04.00+0   DOI: 10.1128/MCB.21.19.6450-6460.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.


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