• 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Molecular and Cellular Biology >The RNA Recognition Motif of Eukaryotic Translation Initiation Factor 3g (eIF3g) Is Required for Resumption of Scanning of Posttermination Ribosomes for Reinitiation on GCN4 and Together with eIF3i Stimulates Linear Scanning
【24h】

The RNA Recognition Motif of Eukaryotic Translation Initiation Factor 3g (eIF3g) Is Required for Resumption of Scanning of Posttermination Ribosomes for Reinitiation on GCN4 and Together with eIF3i Stimulates Linear Scanning

机译：真核翻译起始因子3g（eIF3g）的RNA识别母体是恢复在GCN4上重新终止后核糖体扫描的必需条件，并与eIF3i一起刺激线性扫描

获取原文
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

Recent reports have begun unraveling the details of various roles of individual eukaryotic translation initiation factor 3 (eIF3) subunits in translation initiation. Here we describe functional characterization of two essential Saccharomyces cerevisiae eIF3 subunits, g/Tif35 and i/Tif34, previously suggested to be dispensable for formation of the 48S preinitiation complexes (PICs) in vitro. A triple-Ala substitution of conserved residues in the RRM of g/Tif35 (g/tif35-KLF) or a single-point mutation in the WD40 repeat 6 of i/Tif34 (i/tif34-Q258R) produces severe growth defects and decreases the rate of translation initiation in vivo without affecting the integrity of eIF3 and formation of the 43S PICs in vivo. Both mutations also diminish induction of GCN4 expression, which occurs upon starvation via reinitiation. Whereas g/tif35-KLF impedes resumption of scanning for downstream reinitiation by 40S ribosomes terminating at upstream open reading frame 1 (uORF1) in the GCN4 mRNA leader, i/tif34-Q258R prevents full GCN4 derepression by impairing the rate of scanning of posttermination 40S ribosomes moving downstream from uORF1. In addition, g/tif35-KLF reduces processivity of scanning through stable secondary structures, and g/Tif35 specifically interacts with Rps3 and Rps20 located near the ribosomal mRNA entry channel. Together these results implicate g/Tif35 and i/Tif34 in stimulation of linear scanning and, specifically in the case of g/Tif35, also in proper regulation of the GCN4 reinitiation mechanism.
机译：最近的报道已开始阐明单个真核翻译起始因子3（eIF3）亚基在翻译起始中各种作用的细节。在这里，我们描述了两个必需的酿酒酵母eIF3亚基g / Tif35和i / Tif34的功能表征，这些亚基以前被建议在体外形成48S预起始复合物（PIC） em>。 g / Tif35（ g / tif35-KLF ）的RRM中保守残基的三丙氨酸取代或i / Tif34的WD40重复序列6（ i / tif34-Q258R ）在不影响eIF3完整性和体内43s PICs形成的情况下，会产生严重的生长缺陷并降低其在体内的翻译起始速率。这两个突变也减少了 GCN4 表达的诱导，该诱导在饥饿后通过重新初始化发生。而 g / tif35-KLF 阻止恢复终止于 GCN4 mRNA前导序列 i的上游开放阅读框1（uORF1）的40S核糖体进行下游重新初始化的扫描。 / tif34-Q258R 通过削弱从uORF1向下游移动的终止40S核糖体的扫描速度来防止完全 GCN4 抑制。此外， g / tif35-KLF 会降低通过稳定二级结构进行扫描的过程，并且g / Tif35与位于核糖体mRNA进入通道附近的Rps3和Rps20特异性相互作用。这些结果共同暗示了g / Tif35和i / Tif34会刺激线性扫描，尤其是在g / Tif35的情况下，还可能适当调节 GCN4 重新初始化机制。

著录项

相似文献

  • 外文文献
  • 中文文献
获取原文

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号