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Molecular and Cellular Biology, August 2000, p. 5960-5973, Vol. 20, No. 16
0270-7306/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.
Genetic Interactions between TFIIS and the Swi-Snf
Chromatin-Remodeling Complex
Judith K.
Davie
and
Caroline M.
Kane*
Department of Molecular and Cell Biology,
University of California, Berkeley, California 94720-3202
Received 3 February 2000/Returned for modification 8 March
2000/Accepted 16 May 2000
The eukaryotic transcript elongation factor TFIIS enables RNA
polymerase II to read through blocks to elongation in vitro and
interacts genetically with a variety of components of the transcription
machinery in vivo. In Saccharomyces cerevisiae, the gene
encoding TFIIS (PPR2) is not essential, and disruption strains exhibit only mild phenotypes and an increased sensitivity to
6-azauracil. The nonessential nature of TFIIS encouraged
the use of a synthetic lethal screen to elucidate the in vivo roles of
TFIIS as well as provide more information on other factors involved in
the regulation of transcript elongation. Several genes were identified
that are necessary for either cell survival or robust growth when the
gene encoding TFIIS has been disrupted. These include UBP3,
KEX2, STT4, and SWI2/SNF2. SWI1 and
SNF5 disruptions were also synthetically lethal with
ppr2
, suggesting that the reduced ability to remodel
chromatin confers the synthetic phenotype. The synthetic phenotypes
show marked osmosensitivity and cytoskeletal defects, including a
terminal hyperelongated bud phenotype with the Swi-Snf complex. These
results suggest that genes important in osmoregulation, cell membrane
synthesis and integrity, and cell division may require the Swi-Snf
complex and TFIIS for efficient transcription. The detection of these
genetic interactions provides another functional link between the
Swi-Snf complex and the elongation machinery.
*
Corresponding author. Mailing address: Department of
Molecular and Cell Biology, University of California, Berkeley, CA
94720-3202. Phone: (510) 642-4118. Fax: (510) 643-9290. E-mail:
kanecm{at}uclink4.berkeley.edu.

Present address: University of Texas M.D. Anderson Cancer
Center, Biochemistry/Molecular Biology, Houston, TX
77030.
Molecular and Cellular Biology, August 2000, p. 5960-5973, Vol. 20, No. 16
0270-7306/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.
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