Mutations in SIN4, which encodes a global transcriptional regulator in Saccharomyces cerevisiae, have been suggested to lead to an increase in basal transcription of various genes by causing an alteration in chromatin structure. We reported previously that this activation of basal transcription occurs via a mechanism that differs from activator-mediated transcriptional enhancement. This finding prompted us to seek general activators of basal transcription by screening for extragenic suppressors of a sin4 mutation using PHO5, which is activated by the transcriptional activator Pho4, as a reporter gene. One of the mutations found, the semi-dominant ABE1-1, is described here. The ABE1-1 mutation reduced the enhanced basal transcription of PHO5 caused by the sin4 mutation, but did not impair Pho4-mediated activation of PHO5. The ABE1-1 mutation also suppressed the aggregation phenotype and the rough colony morphology of the sin4 mutant cells, while it exacerbated temperature sensitive growth and telomere shortening, suggesting that Abe1p is involved in the basal transcription not only of PHO5 but also of other diversely regulated genes. SWI1, which encodes a component of the Swi-Snf complex that has chromatin remodeling activity, was identified as a gene-dosage suppressor of the ABE1-1 mutation. ABE1-1 was found to be allelic to GAL11. These observations suggest that Gal11 acts as a general activator for the basal transcription of various genes, possibly by relieving torsional stress in chromatin, and that its function is repressed by the Sin4 protein.

• PMID: 12715155
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Journal Article | Research Support, Non-U.S. Gov't

Authors

Mizuno T, Harashima S

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