Why Ppr1p is a weak activator of transcription

被引:5
作者
Pätzold, AJ [1 ]
Lehming, N [1 ]
机构
[1] Max Planck Gesell, Max Delbruck Lab, D-50829 Cologne, Germany
关键词
Ppr1P; split-ubiquitin; transcription; Tup1p; URA3; Saccharomyces cerevisiae;
D O I
10.1016/S0014-5793(01)02312-2
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Upon uracil depletion, the transcriptional activator Ppr1p stimulates expression of the Saccharomyces cerevisiae URA3 gene only four-fold. We performed a split-ubiquitin screen with Tup1p as bait, and we found that the global repressor Tup1p interacts with the transcriptional activator Ppr1p both in vivo and in vitro, The interaction is biologically significant, since the deletion of the TUP1 gene as well as the removal of the Tup1p-binding domain from Ppr1p results in an increased expression of the URA3 gene. Our results suggest that Tup1p blocks Ppr1p directly, and that Ppr1p is a weak activator of transcription because of its interaction with Tup1p, Thus we were able to demonstrate that the global repressor Tup1p can modulate transcription by interacting with an activator. (C) 2001 Federation of European Biochemical Societies, Published by Elsevier Science B.V. All rights reserved.
引用
收藏
页码:64 / 68
页数:5
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