Collart M A
Department of Medical Biochemistry, University of Geneva Medical School, Switzerland.
Mol Cell Biol. 1996 Dec;16(12):6668-76. doi: 10.1128/MCB.16.12.6668.
Previous studies demonstrated that mutations in the Saccharomyces cerevisiae NOT genes increase transcription from TATA-less promoters. In this report, I show that in contrast, mutations in the yeast MOT1 gene decrease transcription from TATA-less promoters. I also demonstrate specific genetic interactions between the Not complex, Mot1p, and another global regulator of transcription in S. cerevisiae, Spt3p. Five distinct genetic interactions have been established. First, a null allele of SPT3, or a mutation in SPT15 that disrupts the interaction between Spt3p and TATA-binding protein (TBP), allele specifically suppressed the not1-2 mutation. Second, in contrast to not mutations, mutations in MOT1 decreased HIS3 and HIS4 TATA-less transcription. Third, not mutations suppressed toxicity due to overexpression of TBP in mot1-1 mutants. Finally, overexpression of SPT3 caused a weak Not- mutant phenotype in mot1-1 mutants. Collectively, these results suggest a novel type of transcriptional regulation whereby the distribution of limiting TBP (TFIID) on weak and strong TBP-binding core promoters is regulated: Mot1p releases stably bound TBP to allow its redistribution to low-affinity sites, and the Not proteins negatively regulate the activity of factors such as Spt3p that favor distribution of TBP to these low-affinity sites.
先前的研究表明,酿酒酵母NOT基因中的突变会增加无TATA框启动子的转录。在本报告中,我发现相反,酵母MOT1基因中的突变会减少无TATA框启动子的转录。我还证明了Not复合物、Mot1p与酿酒酵母中另一种全局转录调节因子Spt3p之间存在特定的遗传相互作用。已建立了五种不同的遗传相互作用。首先,SPT3的无效等位基因,或SPT15中破坏Spt3p与TATA结合蛋白(TBP)之间相互作用的突变,特异性地抑制了not1-2突变。其次,与not突变相反,MOT1中的突变降低了HIS3和HIS4无TATA框的转录。第三,not突变抑制了mot1-1突变体中由于TBP过表达导致的毒性。最后,SPT3的过表达在mot1-1突变体中引起了弱的Not-突变体表型。总的来说,这些结果提示了一种新型的转录调控方式,即限制TBP(TFIID)在弱和强TBP结合核心启动子上的分布受到调控:Mot1p释放稳定结合的TBP以使其重新分布到低亲和力位点,而Not蛋白负向调节诸如Spt3p等有利于TBP分布到这些低亲和力位点的因子的活性。