A yeast taf17 mutant requires the Swi6 transcriptional activator for viability and shows defects in cell cycle-regulated transcription

Citation
N. Macpherson et al., A yeast taf17 mutant requires the Swi6 transcriptional activator for viability and shows defects in cell cycle-regulated transcription, GENETICS, 154(4), 2000, pp. 1561-1576
Citations number
84
Categorie Soggetti
Biology,"Molecular Biology & Genetics
Journal title
GENETICS
ISSN journal
00166731 → ACNP
Volume
154
Issue
4
Year of publication
2000
Pages
1561 - 1576
Database
ISI
SICI code
0016-6731(200004)154:4<1561:AYTMRT>2.0.ZU;2-K
Abstract
In Saccharomyces cerevisiae, the Swi6 protein is a component of two transcr iption factors, SBF and MBF, that promote expression of a large group of ge nes in the late G1 phase of the cell cycle. Although SBF is required for ce ll viability, SW16 is not an essential gene. We performed a synthetic letha l screen to identify genes required for viability in the absence of SWI6 an d identified 10 complementation groups of swi6-dependent lethal mutants, de signated SLM1 through SLM10. We were most interested in mutants showing a c ell cycle arrest phenotype; both slm7-1 swi6 Delta and slm8-1 swi6 Delta do uble mutants accumulated as large, unbudded cells with increased 1N DNA con tent and showed a temperature-sensitive growth arrest in the presence of Sw i6. Analysis of the transcript levels of cell cycle-regulated genes in slm7 -1 SWI6 mutant strains at the permissive temperature revealed defects in re gulation of a subset of cyclin-encoding genes. Complementation and allelism tests showed that SLM7 is allelic with the TAF17 gene, which encodes a his tone-like component of the general transcription factor TFIID and the SAGA histone acetyltransferase complex. Sequencing showed that the slm7-1 allele of TAF17 is predicted to encode a version of Taf17 that is truncated withi n a highly conserved region. The cell cycle and transcriptional defects cau sed by taf17(sim7-1) are consistent with the role of TAF(II)s as modulators of transcriptional activation and may reflect a role for TAF17 in regulati ng activation by SBF and MBF.