Yeast Genetics and Molecular Biology 1998
College Park, Maryland
August 1998


Name: Sudarsanam, Priya
Mailing Address: Department of Genetics, Harvard Medical School, 200, Longwood Avenue, Boston, MA 02115, USA
Email Address: sudarsanam@rascal.med.harvard.edu
Phone and Fax numbers: (617) 432-7558, (617) 432-7663

014

Analysis of Snf/Swi function in S. cerevisiae .


Priya Sudarsanam (1) , Vishwanath R. Iyer (2), Yixue Cao (3), Brehon C. Laurent (3), Patrick O. Brown (2), Fred Winston (1)
(1) Department of Genetics, Harvard Medical School, 200, Longwood Avenue, Boston, MA 02115, USA; (2) Department of Biochemistry, Stanford University School of Medicine, Howard Hughes Medical Institute, Stanford, CA 94305, USA; (3) Department of Microbiology and Immunology, State University of New York, Brooklyn, NY 11203, USA

A number of studies previously suggested that the Snf/Swi complex of S. cerevisiae remodels nucleosomes to help transcription factors bind to their sites. We have taken three different strategies to learn about Snf/Swi function in vivo . First, to determine how many genes require Snf/Swi for normal transcription, we have used DNA microarrays to study the effect of snf/swi null mutations on mRNA levels of the entire yeast genome. Less than three percent of all mRNAs are altered by at least three-fold. While most affected mRNAs decrease in level, some mRNAs show increases. In addition, cells grown in rich media show a different pattern than cells grown in minimal media. Second, we have examined if the transcription of one Snf/Swi-dependent gene, SUC2 , is also controlled by the histone acetyltransferase Gcn5. Previous genetic evidence suggested that Snf/Swi and Gcn5 may be partially redundant for transcriptional activation. Our results have shown that in the absence of either function, SUC2 mRNA levels are greatly reduced, well below that found in either single mutant. Finally, we have studied the requirement for Snf/Swi in the establishment and maintenance of SUC2 transcription. Our studies suggest that Snf/Swi is required for both establishment and maintenance of a fully active SUC2 promoter. In summary, the requirement for Snf/Swi occurs at a number of promoters in vivo and its role in overcoming repression by nucleosomes is at least partially redundant with that of Gcn5.


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