Antagonistic Controls of Chromatin and mRNA Start Site Selection by Tup Family Corepressors and the CCAAT-Binding Factor

Ryuta Asada; Naomichi Takemata; Charles S. Hoffman; Kunihiro Ohta; Kouji Hirota

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Antagonistic Controls of Chromatin and mRNA Start Site Selection by Tup Family Corepressors and the CCAAT-Binding Factor

机译：Tup家族的presspressors和CCAAT结合因子的染色质和mRNA起始站点选择的拮抗控制。

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The Tup family corepressors contribute to critical cellular responses, such as the stress response and differentiation, presumably by inducing repressive chromatin, though the precise repression mechanism remains to be elucidated. The Schizosaccharomyces pombe fission yeast Tup family corepressors Tup11 and Tup12 (Tup11/12), which are orthologs of Tup1 in Saccharomyces cerevisiae budding yeast and Groucho in Drosophila, negatively control chromatin and the transcriptional activity of some stress-responsive genes. Here, we demonstrate that Tup11/12 repress transcription of a gluconeogenesis gene, fbp1+, by three distinct mechanisms. First, Tup11/12 inhibit chromatin remodeling in the fbp1+ promoter region where the Atf1 and Rst2 transcriptional activators bind. Second, they repress the formation of an open chromatin configuration at the fbp1+ TATA box. Third, they repress mRNA transcription per se by regulating basic transcription factors. These inhibitory actions of Tup11/12 are antagonized by three different types of transcriptional activators: CREB/ATF-type Atf1, C₂H₂ zinc finger-type Rst2, and CBF/NF-Y-type Php5 proteins. We also found that impaired chromatin remodeling and fbp1+mRNA transcription in php5Δ strains are rescued by the double deletions of tup11+ and tup12+, although the distribution of the transcription start sites becomes broader than that in wild-type cells. These data reveal a new mechanism of precise determination of the mRNA start site by Tup family corepressors and CBF/NF-Y proteins.

机译：尽管尚需阐明确切的阻抑机制，但Tup家族的核心抑制剂可能通过诱导抑制性染色质来促进关键的细胞反应，例如应激反应和分化。裂殖酵母裂殖酵母Tup家族的共抑制子Tup11和Tup12（Tup11 / 12）是果蝇酿酒酵母中的Tup1直向同源物，与果蝇中的Groucho同源，对染色质和某些应激反应基因的转录活性产生负面影响。在这里，我们证明Tup11 / 12通过三种不同的机制抑制糖异生基因 fbp1 + 的转录。首先，Tup11 / 12抑制Atf1和Rst2转录激活因子结合的 fbp1 + 启动子区域中的染色质重塑。其次，他们抑制在 fbp1 + TATA盒中开放的染色质构型的形成。第三，它们通过调节基本转录因子来抑制mRNA转录本身。 Tup11 / 12的这些抑制作用被三种不同类型的转录激活剂拮抗：CREB / ATF型Atf1，C _{2 H _{2 锌指型Rst2和CBF / NF-Y型Php5蛋白。我们还发现， php5 Δ菌株中染色质重塑受损和 fbp1 + mRNA转录可通过双重缺失得到挽救。尽管 tup11 + 和 tup12 + 转录起始位点的分布比野生型细胞更宽。这些数据揭示了一种新的机制，可以通过Tup家族的心脏加压因子和CBF / NF-Y蛋白精确确定mRNA的起始位点。}} 展开▼

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《Molecular and Cellular Biology》 |2015年第5期|共9页

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Ryuta Asada; Naomichi Takemata; Charles S. Hoffman; Kunihiro Ohta; Kouji Hirota;
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中图分类细胞生物学;

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1. Reciprocal Nuclear Shuttling of Two Antagonizing Zn Finger Proteins Modulates Tup Family Corepressor Function To Repress Chromatin Remodeling [J] . Kouji Hirota, Charles S. Hoffman, Kunihiro Ohta Eukaryotic cell . 2006,第12期

机译：两个拮抗的锌指蛋白的互惠核梭调节Tup家族corepressor功能，以抑制染色质重塑。

2. Recruitment and delivery of the fission yeast Rst2 transcription factor via a local genome structure counteracts repression by Tup1-family corepressors [J] . Nucleic Acids Research . 2017,第16期

机译：通过局部基因组结构募集和递送裂变酵母RST2转录因子Tup1-Family CoreCressors的抑制

3. Recruitment and delivery of the fission yeast Rst2 transcription factor via a local genome structure counteracts repression by Tup1-family corepressors [J] . Hiroshi Iwasaki, Charles S. Hoffman, Ryuta Asada, Nucleic acids research . 2017,第16期

机译：通过局部基因组结构招募和传递裂变酵母Rst2转录因子抵消了Tup1家族共表达的抑制

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6. Antagonistic Controls of Chromatin and mRNA Start Site Selection by Tup Family Corepressors and the CCAAT-Binding Factor [O] . Ryuta Asada, Naomichi Takemata, Charles S. Hoffman, 2015

机译：Tup家族的presspressors和CCAAT结合因子的染色质和mRNA起始站点选择的拮抗控制。

7. Reciprocal Nuclear Shuttling of Two Antagonizing Zn Finger Proteins Modulates Tup Family Corepressor Function To Repress Chromatin Remodeling▿ [O] . Hirota, Kouji, Hoffman, Charles S., Ohta, Kunihiro 2006

机译：两种拮抗锌指蛋白的相互核穿梭调节Tup家族的corepressor功能，以抑制染色质重塑▿

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机译：控制引物退火，以提高核酸扩增试剂盒中退火的特异性。扩增DNA或核酸混合物的核酸序列的方法以及选择性扩增靶DNA或核酸混合物的核酸序列的方法用于检测DNA与两个或多个核酸样品中差异表达的mRNA的互补性的方法，扩增cDNA和DNA片段的方法可快速靶向。全长与mRNA cDNA互补的双细丝cDNA的cDNA群体，以及与mRNA互补的5'增强双细丝的cDNA，同时扩增而不是核苷酸靶序列的方法，产生数字印刷gDNA DNA的方法mRNA样品中的RNA和RNA.mRNA样品的多基因家族中用于鉴定同源片段的方法是保守的，这是一种在靶标中诱变的方法

4. Control primer annealing to improve the specificity of annealing in nucleic acid amplification, kit, methods for amplifying nucleic acid sequences of DNA and sequence of target nucleic acid or a mixture of nucleic acids, to detect the complementari Dade of DNA to mRNA differentially expressed in two or more samples of nucleic acid.To amplify a fragment of the cDNA target quickly, to amplify a population of cDNAs of filament double full-length complementary to mRNAs cDNAs, and filament double fortified with 5 'complementary to mRNAs to amplify rather than a sequence of nucleotide al VO at the same time, to produce a digital printing gDNA DNA, and RNA in a sample of mRNA.To identify segments of homology is conserved in a multigene family from a sample of mRNA, to identify a variation of nucleotide in a target nucleic acid, for mutagenesis in a target nucleic acid, and use of the initiator [P] . 外国专利： BRPI0214741B1 . 2015-05-12

机译：控制引物退火以改善核酸扩增中退火的特异性，试剂盒，扩增DNA核酸序列和靶核酸序列或核酸混合物的方法，检测DNA与mRNA互补表达的互补性（两种）或更多核酸样品。要快速扩增cDNA靶标的片段，以扩增与mRNA cDNA互补的长丝两倍全长的cDNA群体，并用与mRNA互补的5'双重修饰的长丝进行扩增而不是序列同时鉴定一个核苷酸的VO片段，以产生一个数字印刷的gDNA DNA和一个mRNA样品中的RNA。从一个mRNA样品中鉴定一个多基因家族中的同源片段是保守的，以鉴定一个核苷酸中一个核苷酸的变异。靶核酸，用于在靶核酸中诱变，以及引发剂的用途

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机译：编码RNA，蛋白质，多肽或肽的修饰基因，载体，控制基因中蛋白质，多肽或肽的产生，修饰基因，去除5'-帽结构和/或3'-的方法从基因转录的前mRNA或mRNA的滑轮尾，用于控制细胞内蛋白质，多肽或肽的产生，进化和体外选择，以产生配体结合的RNA进化和体外选择序列用于生产依赖配体的自切割RNA序列，合成DNA分子，配体和修饰基因的组合，dna和依赖配体的自切割合成RNA分子

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Antagonistic Controls of Chromatin and mRNA Start Site Selection by Tup Family Corepressors and the CCAAT-Binding Factor

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