Genetics, Vol. 154, 1561-1576, April 2000, Copyright © 2000

A Yeast taf17 Mutant Requires the Swi6 Transcriptional Activator for Viability and Shows Defects in Cell Cycle-Regulated Transcription

Neil Macphersona, Vivien Measdaya, Lynda Moorea, and Brenda Andrewsa
a Department of Molecular and Medical Genetics, University of Toronto, Toronto, Ontario M55 1A8, Canada

Corresponding author: Brenda Andrews, Department of Molecular and Medical Genetics, University of Toronto, Rm. 4285, Medical Sciences Bldg., 1 King's College Circle, Toronto, Ontario M5S 1A8, Canada., brenda.andrews{at}utoronto.ca (E-mail)

Communicating editor: A. P. MITCHELL

In Saccharomyces cerevisiae, the Swi6 protein is a component of two transcription factors, SBF and MBF, that promote expression of a large group of genes in the late G1 phase of the cell cycle. Although SBF is required for cell viability, SWI6 is not an essential gene. We performed a synthetic lethal screen to identify genes required for viability in the absence of SWI6 and identified 10 complementation groups of swi6-dependent lethal mutants, designated SLM1 through SLM10. We were most interested in mutants showing a cell cycle arrest phenotype; both slm7-1 swi6{Delta} and slm8-1 swi6{Delta} double mutants accumulated as large, unbudded cells with increased 1N DNA content and showed a temperature-sensitive growth arrest in the presence of Swi6. Analysis of the transcript levels of cell cycle-regulated genes in slm7-1 SWI6 mutant strains at the permissive temperature revealed defects in regulation of a subset of cyclin-encoding genes. Complementation and allelism tests showed that SLM7 is allelic with the TAF17 gene, which encodes a histone-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 within a highly conserved region. The cell cycle and transcriptional defects caused by taf17slm7-1 are consistent with the role of TAFIIs as modulators of transcriptional activation and may reflect a role for TAF17 in regulating activation by SBF and MBF.





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