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Activation of basal transcription by a mutation in SIN4, a yeast global repressor, occurs through a mechanism different from activator-mediated transcriptional enhancement

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Abstract

The Saccharomyces cerevisiae protein Sin4 has been suggested to affect the transcription of various genes by locally altering chromatin structure. Previous studies have defined two classes of promoters: those which are activated by loss of SIN4 function (termed sin4-responsive promoters) and those which are not activated by sin4 mutations (termed sin4 non-responsive promoters). We analyzed the mechanism of this differential response of the two classes of promoters to a sin4 mutation. The sin4 non-responsive promoters were activated when upstream elements in the promoter region were eliminated. The upstream elements of sin4 non-responsive promoters were, in turn, found to repress the activity of the sin4-responsive promoters in an orientation-independent manner. The sin4-mediated activation was repressed by the Rme1- but not by the Tup1-Ssn6-mediated repression system. Activation of sin4-responsive promoters by Pho4 and the sin4 mutation was additive, and enhancement of transcription driven by sin4-responsive promoters was found to be due to an increase in the basal rate of transcription. The upstream regions in the sin4 non-responsive promoters contained elements that were able to inhibit activation of basal transcription. Based on these observations, we suggest that activation of basal transcription by a mutation in a gene for a global repressor, SIN4, occurs through a mechanism that differs from that responsible for activator-mediated transcriptional enhancement, and we therefore propose that basal transcription and activator-mediated transcription are repressed by different mechanisms.

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Received: 4 May 1999 / Accepted: 21 September 1999

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Mizuno, T., Harashima, S. Activation of basal transcription by a mutation in SIN4, a yeast global repressor, occurs through a mechanism different from activator-mediated transcriptional enhancement. Mol Gen Genet 263, 48–59 (2000). https://doi.org/10.1007/PL00008675

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  • DOI: https://doi.org/10.1007/PL00008675

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