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Originally published as Genetics Published Articles Ahead of Print on August 22, 2005.

Genetics, Vol. 171, 959-973, November 2005, Copyright © 2005
doi:10.1534/genetics.105.046557

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TFIID and Spt-Ada-Gcn5-Acetyltransferase Functions Probed by Genome-wide Synthetic Genetic Array Analysis Using a Saccharomyces cerevisiae taf9-ts Allele

Elena Milgrom1, Robert W. West, Jr.1, Chen Gao1 and W.-C. Winston Shen2

Department of Biochemistry and Molecular Biology, State University of New York Upstate Medical University, Syracuse, New York 13210

2 Corresponding author: Department of Biochemistry and Molecular Biology, State University of New York, Upstate Medical University, 750 E. Adams St., WHA Room 4281, Syracuse, NY 13210.
E-mail: shenw{at}upstate.edu

TAF9 is a TATA-binding protein associated factor (TAF) conserved from yeast to humans and shared by two transcription coactivator complexes, TFIID and SAGA. The essentiality of the TAFs has made it difficult to ascertain their roles in TFIID and SAGA function. Here we performed a genomic synthetic genetic array analysis using a temperature-sensitive allele of TAF9 as a query. Results from this experiment showed that TAF9 interacts genetically with: (1) genes for multiple transcription factor complexes predominantly involving Mediator, chromatin modification/remodeling complexes, and regulators of transcription elongation; (2) virtually all nonessential genes encoding subunits of the SWR-C chromatin-remodeling complex and both TAF9 and SWR-C required for expressing the essential housekeeping gene RPS5; and (3) key genes for cell cycle control at the G1/S transition, as well as genes involved in cell polarity, cell integrity, and protein synthesis, suggesting a link between TAF9 function and cell growth control. We also showed that disruption of SAGA by deletion of SPT20 alters histone-DNA contacts and phosphorylated forms of RNA polymerase II at coding sequences. Our results raise the possibility of an unappreciated role for TAF9 in transcription elongation, perhaps in the context of SAGA, and provide further support for TAF9 involvement in cell cycle progression and growth control.




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