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

Content Provider	Springer Nature Link
Author	Mizu, T. Harashima, S.
Copyright Year	2000
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.
Starting Page	48
Ending Page	59
Page Count	12
File Format	PDF
ISSN	00268925
Journal	Molecular and General Genetics MGG
Volume Number	263
Issue Number	1
e-ISSN	14321874
Language	English
Publisher	Springer-Verlag
Publisher Date	2000-02-23
Publisher Place	Berlin/Heidelberg
Access Restriction	Subscribed
Content Type	Text
Resource Type	Article
Subject	Genetics

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