The structure and function of a novel G protein family regulating eukaryotic mRNA dynamics

调节真核mRNA动态的新型G蛋白家族的结构和功能

基本信息

  • 批准号:
    13854025
  • 负责人:
  • 金额:
    $ 78.87万
  • 依托单位:
  • 依托单位国家:
    日本
  • 项目类别:
    Grant-in-Aid for Scientific Research (S)
  • 财政年份:
    2001
  • 资助国家:
    日本
  • 起止时间:
    2001 至 2005
  • 项目状态:
    已结题

项目摘要

In eukaryotic protein synthesis, all three termination codons are directly recognized by a polypeptide-chain releasing factor, eRF1,to release polypeptide chain from ribosome, and another releasing factor, eRF3,is required for eRF1 binding to ribosomal A site. We previously reported that a GTP-binding protein, whose carboxy-terminal sequence is homologous to the eukaryotic elongation factor EF1α, forms a complex with eRF1 to function as eRF3 in the translation termination and that eRF3 consists of the EF1α-like carboxy-terminal (C) and amino-terminal (N) domains. In the present studies, we investigated the structures and functions of eRF3 and its related G proteins. The major findings obtained in this study are summarized as follows.1)The C domain of eRF3 associated with eRF1,whereas the N domain was capable of binding to poly-adenylate binding protein (PABP) associating with the poly(A) tail of mRNAs presumably for their stabilization. 2)When the interaction between eRF3-N domain and PABP was abolished, decay rate of all mRNAs was decreased due to the inhibition of poly(A) tail shortening. 3)We identified a poly(A) nuclease (PAN) complex that is activated by PABP and found that eRF3 and PAN complex competitively bound to PABP. These results indicate that the translation termination-coupled mRNA decay is mediated through eRF3-dependent poly(A) shortening. Thus, eRF3 functions not only as an eRF1-carrier protein in the translation termination but also as an initiator of the mRNA degradation machinery. 4)We also investigated the functions of other G proteins (Ski7 and eRFS) structurally related to eRF3 and found that the N domains of these G proteins commonly interact with factors involved in mRNA-degradation machineries to regulate mRNA stabilization.
在真核生物的蛋白质合成中,所有三个终止密码子都被一个多肽链释放因子eRF 1直接识别,从而从核糖体释放多肽链,另一个释放因子eRF 3是eRF 1与核糖体A位点结合所必需的。我们以前报道过一个GTP结合蛋白,其羧基端序列与真核细胞延伸因子EF 1 α同源,与eRF 1形成复合物,在翻译终止中起eRF 3的作用,eRF 3由EF 1 α样的羧基端(C)和氨基端(N)结构域组成。本研究对eRF 3及其相关G蛋白的结构和功能进行了研究。主要研究结果如下:1)eRF 3的C结构域与eRF 1结合,而N结构域能够与多聚腺苷酸结合蛋白(PABP)结合,PABP与mRNA的poly(A)尾结合,推测是为了稳定mRNA。2)当eRF 3-N结构域与PABP之间的相互作用被消除时,由于poly(A)尾缩短的抑制,所有mRNA的衰减速率都降低。3)我们鉴定了PABP激活的多聚A核酸酶(PAN)复合物,发现eRF 3和PAN复合物竞争性结合PABP。这些结果表明,翻译终止偶联的mRNA衰变是通过eRF 3依赖性poly(A)缩短介导的。因此,eRF 3不仅在翻译终止中作为eRF 1载体蛋白,而且还作为mRNA降解机制的启动子。4)我们还研究了与eRF 3结构相关的其他G蛋白(Ski 7和eRFS)的功能,发现这些G蛋白的N结构域通常与参与mRNA降解机制的因子相互作用,以调节mRNA的稳定性。

项目成果

期刊论文数量(77)
专著数量(0)
科研奖励数量(0)
会议论文数量(0)
专利数量(0)
堅田 利明: "翻訳終結とmRNA分解を結ぶGタンパク質"学術月報. 56. 1258-1262 (2003)
Toshiaki Katata:“连接翻译终止和 mRNA 降解的 G 蛋白”学术月刊报告 56. 1258-1262 (2003)。
  • DOI:
  • 发表时间:
  • 期刊:
  • 影响因子:
    0
  • 作者:
  • 通讯作者:
H.Kurosu, T.Katada: "Association of phosphatidylinositol 3-kinase composed of p11Oβ-catalytic and p85-regulatory subunits with the small GTPase Rab5"J.Biochem.. 130. 73-78 (2001)
H.Kurosu, T.Katada:“由 p11Oβ 催化和 p85 调节亚基组成的磷脂酰肌醇 3-激酶与小 GTPase Rab5 的关联”J.Biochem.. 130. 73-78 (2001)
  • DOI:
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  • 期刊:
  • 影响因子:
    0
  • 作者:
  • 通讯作者:
K.Kontani, M.Tada, T.Ogawa, T.Okai, K.Saito, Y.Araki, T.Katada: "Di-Ras : A distinct subgroup of Ras-family GTPases with unique biochemical properties"J.Biol.Chem.. 277. 41070-41078 (2002)
K.Kontani、M.Tada、T.Okawa、T.Okai、K.Saito、Y.Araki、T.Katada:“Di-Ras:具有独特生化特性的 Ras 家族 GTP 酶的独特亚组”J.Biol。
  • DOI:
  • 发表时间:
  • 期刊:
  • 影响因子:
    0
  • 作者:
  • 通讯作者:
Cell fusion : EFF is enough.
细胞融合:EFF就足够了。
  • DOI:
  • 发表时间:
    2005
  • 期刊:
  • 影响因子:
    0
  • 作者:
    Kontani K;et al.
  • 通讯作者:
    et al.
Ski7p G protein interacts with the exosome and the Ski complex for 3′-to-5′ mRNA decay in yeast
  • DOI:
    10.1093/emboj/20.17.4684
  • 发表时间:
    2001-09-03
  • 期刊:
  • 影响因子:
    11.4
  • 作者:
    Araki, Y;Takahashi, S;Katada, T
  • 通讯作者:
    Katada, T
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KATADA Toshiaki其他文献

KATADA Toshiaki的其他文献

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{{ truncateString('KATADA Toshiaki', 18)}}的其他基金

Identification of signaling pathways involved in fungal pathogenicity and search for novel targets for antifungal drugs
鉴定真菌致病性信号通路并寻找抗真菌药物新靶点
  • 批准号:
    20K06550
  • 财政年份:
    2020
  • 资助金额:
    $ 78.87万
  • 项目类别:
    Grant-in-Aid for Scientific Research (C)
Nutrient response mediated by a TRIM-NHL protein
TRIM-NHL 蛋白介导的营养反应
  • 批准号:
    16K14693
  • 财政年份:
    2016
  • 资助金额:
    $ 78.87万
  • 项目类别:
    Grant-in-Aid for Challenging Exploratory Research
A novel signal transduction pathway which regulates the structure of P-body and the dynamics of ARE-mRNAs
调节 P-body 结构和 ARE-mRNA 动态的新型信号转导途径
  • 批准号:
    22659015
  • 财政年份:
    2010
  • 资助金额:
    $ 78.87万
  • 项目类别:
    Grant-in-Aid for Challenging Exploratory Research
Regulation of intracellular vesicle transport by small GTPase cycles
小 GTP 酶循环调节细胞内囊泡运输
  • 批准号:
    20247011
  • 财政年份:
    2008
  • 资助金额:
    $ 78.87万
  • 项目类别:
    Grant-in-Aid for Scientific Research (A)
Membrane-Transport Signaling Involving the GTPase Cycle of G proteins
涉及 G 蛋白 GTP 酶循环的膜运输信号转导
  • 批准号:
    18207008
  • 财政年份:
    2006
  • 资助金额:
    $ 78.87万
  • 项目类别:
    Grant-in-Aid for Scientific Research (A)
Functional analysis of atypical G proteins involved in cell signaling network
参与细胞信号网络的非典型G蛋白的功能分析
  • 批准号:
    17079002
  • 财政年份:
    2005
  • 资助金额:
    $ 78.87万
  • 项目类别:
    Grant-in-Aid for Scientific Research on Priority Areas
New research initiatives in the study of G-protein signaling systems integrating cell communication network
整合细胞通讯网络的G蛋白信号系统研究新举措
  • 批准号:
    17079001
  • 财政年份:
    2005
  • 资助金额:
    $ 78.87万
  • 项目类别:
    Grant-in-Aid for Scientific Research on Priority Areas
G protein-dependent vectorial transportation of receptors, ion channels, and transporters
受体、离子通道和转运蛋白的 G 蛋白依赖性载体运输
  • 批准号:
    12144202
  • 财政年份:
    2000
  • 资助金额:
    $ 78.87万
  • 项目类别:
    Grant-in-Aid for Scientific Research on Priority Areas
Physiological roles of cell surface ecto-enzymes
细胞表面胞外酶的生理作用
  • 批准号:
    11694249
  • 财政年份:
    1999
  • 资助金额:
    $ 78.87万
  • 项目类别:
    Grant-in-Aid for Scientific Research (B).
Analysis of the functions of G protein βγ-Subunit and application to drug design
G蛋白βγ亚基的功能分析及其在药物设计中的应用
  • 批准号:
    10557220
  • 财政年份:
    1998
  • 资助金额:
    $ 78.87万
  • 项目类别:
    Grant-in-Aid for Scientific Research (B)

相似海外基金

Elucidating premature translation termination in Cystic Fibrosis
阐明囊性纤维化中的过早翻译终止
  • 批准号:
    10362522
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    2020
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    $ 78.87万
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Study of molecular mechanisms for translation termination and ribosome recycling by eukaryotic ribosome
真核核糖体翻译终止和核糖体回收的分子机制研究
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    20H03180
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    2020
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    $ 78.87万
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Analysis of post-translation termination event
翻译后终止事件分析
  • 批准号:
    20H03438
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    2020
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Molecular mechanisms of translation termination in bacteria
细菌翻译终止的分子机制
  • 批准号:
    1907273
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    2019
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    $ 78.87万
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    Standard Grant
Translation termination in human mitochondria: Why do we need four release factors? (A14*)
人类线粒体的翻译终止:为什么我们需要四种释放因子?
  • 批准号:
    405771880
  • 财政年份:
    2018
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Genetic Modifiers of Eukaryotic Translation Termination
真核翻译终止的遗传修饰剂
  • 批准号:
    406511
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    2018
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    Studentship Programs
Development of real-time imaging of local translation at neuronal synapse by using molecular interaction between translation termination factors
利用翻译终止因子之间的分子相互作用开发神经元突触局部翻译的实时成像
  • 批准号:
    15K14319
  • 财政年份:
    2015
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翻译终止的分子原理
  • 批准号:
    8818358
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Molecular principles of translation termination
翻译终止的分子原理
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Mechanism of Translation Termination
翻译终止机制
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    1158127
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    2012
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    $ 78.87万
  • 项目类别:
    Continuing Grant
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