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
- 来源:
- 关键词:
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:
- 发表时间:
- 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:
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
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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
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$ 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)
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