Deluen Cécile, James Nicole, Maillet Laurent, Molinete Miguel, Theiler Grégory, Lemaire Marc, Paquet Nicole, Collart Martine A
Département de Biochimie Médicale, CMU, 1211 Geneva 4, Switzerland.
Mol Cell Biol. 2002 Oct;22(19):6735-49. doi: 10.1128/MCB.22.19.6735-6749.2002.
The Saccharomyces cerevisiae Ccr4-Not complex is a global regulator of transcription that is thought to regulate TATA binding protein (TBP) function at certain promoters specifically. In this paper, we show interactions between the essential domain of Not1p, which interacts with Not4p and Not5p, and the N-terminal domain of yTAF1. We isolated a temperature-sensitive nonsense allele of TAF1, taf1-4, which is synthetically lethal at the permissive temperature when combined with not4 and not5 mutants and which produces high levels of a C-terminally truncated yTAF1 derivative. Overexpression of C-terminally truncated yTAF1 is toxic in not4 or not5 mutants, whereas overexpression of full-length yTAF1 suppresses not4. Furthermore, mutations in the autoinhibitory N-terminal TAND domain of yTAF1 suppress not5, and the overexpression of similar mutants does not suppress not4. We find that, like Not5p, yTAF1 acts as a repressor of stress response element-dependent transcription. Finally, we have evidence for stress-regulated occupancy of promoter DNA by Not5p and for Not5p-dependent regulation of yTAF1 association with promoter DNA. Taken together with our finding that Not1p copurifies with glutathione S-transferase-yTaf1 in large complexes, these results provide the first molecular evidence that the Ccr4-Not complex might interact with yTAF1 to regulate its association at promoters, a function that might in turn regulate the autoinhibitory N-terminal domain of yTAF1.
酿酒酵母Ccr4-Not复合物是一种全局转录调节因子,被认为在某些启动子上特异性调节TATA结合蛋白(TBP)的功能。在本文中,我们展示了与Not4p和Not5p相互作用的Not1p的必需结构域与yTAF1的N端结构域之间的相互作用。我们分离出了TAF1的一个温度敏感型无义等位基因taf1-4,当它与not4和not5突变体结合时,在允许温度下是合成致死的,并且会产生高水平的C端截短的yTAF1衍生物。C端截短的yTAF1的过表达在not4或not5突变体中是有毒的,而全长yTAF1的过表达则抑制not4。此外,yTAF1自抑制性N端TAND结构域中的突变抑制not5,而类似突变体的过表达则不抑制not4。我们发现,与Not5p一样,yTAF1作为应激反应元件依赖性转录的抑制因子发挥作用。最后,我们有证据表明Not5p对启动子DNA的结合受应激调节,以及Not5p对yTAF1与启动子DNA结合的依赖性调节。结合我们发现Not1p在大复合物中与谷胱甘肽S-转移酶-yTaf1共纯化的结果,这些结果提供了首个分子证据,表明Ccr4-Not复合物可能与yTAF1相互作用以调节其在启动子上的结合,这一功能可能反过来调节yTAF1的自抑制性N端结构域。