Suppr超能文献

酵母U6 RNA的5'茎环结构破坏可在体内诱导该RNA聚合酶III转录本的三甲基鸟苷加帽。

Disruption of the 5' stem-loop of yeast U6 RNA induces trimethylguanosine capping of this RNA polymerase III transcript in vivo.

作者信息

Kwan S, Gerlach V L, Brow D A

机构信息

Department of Biomolecular Chemistry, University of Wisconsin Medical School, Madison 53706-1532, USA.

出版信息

RNA. 2000 Dec;6(12):1859-69. doi: 10.1017/s1355838200991325.

Abstract

Primary transcripts made by RNA polymerase II (Pol II), but not Pol I or Pol III, are modified by addition of a 7-methylguanosine (m7G) residue to the triphosphate 5' end shortly after it emerges from the polymerase. The m7G "caps" of small nuclear and small nucleolar RNAs, but not messenger RNAs, are subsequently hypermethylated to a 2,2,7-trimethylguanosine (TMG) residue. U6 RNA, the only small nuclear RNA synthesized by Pol III in most eukaryotes, does not receive a methylguanosine cap. However, human U6 RNA is O-methylated on the 5'-terminal (gamma) phosphate by an enzyme that recognizes the 5' stem-loop of U6. Here we show that variant yeast U6 RNAs truncated or substituted within the 5' stem-loop are TMG capped in vivo. Accumulation of the most efficiently TMG-capped U6 RNA variant is strongly inhibited by a conditional mutation in the largest subunit of Pol III, confirming that it is indeed synthesized by Pol III. Thus, methylguanosine capping and cap hypermethylation are not exclusive to Pol II transcripts in yeast. We propose that TMG capping of variant U6 RNAs occurs posttranscriptionally due to exposure of the 5' triphosphate by disruption of protein binding and/or gamma-methyl phosphate capping. 5' truncation and TMG capping of U6 RNA does not appear to affect its normal function in splicing, suggesting that assembly and action of the spliceosome is not very sensitive to the 5' end structure of U6 RNA.

摘要

由RNA聚合酶II(Pol II)而非Pol I或Pol III产生的初级转录本,在从聚合酶中出现后不久,会通过在三磷酸5'端添加一个7-甲基鸟苷(m7G)残基进行修饰。小核RNA和小核仁RNA的m7G“帽”会随后被超甲基化为2,2,7-三甲基鸟苷(TMG)残基,而信使RNA则不会。U6 RNA是大多数真核生物中由Pol III合成的唯一小核RNA,它不会获得甲基鸟苷帽。然而,人类U6 RNA在5'-末端(γ)磷酸上被一种识别U6 5'茎环的酶进行O-甲基化。在这里我们表明,在5'茎环内被截断或替换的变异酵母U6 RNA在体内被TMG加帽。最有效地被TMG加帽的U6 RNA变异体的积累受到Pol III最大亚基的条件性突变的强烈抑制,证实它确实是由Pol III合成的。因此,甲基鸟苷加帽和帽超甲基化在酵母中并非Pol II转录本所特有。我们提出,变异U6 RNA的TMG加帽是在转录后发生的,这是由于蛋白质结合的破坏和/或γ-甲基磷酸加帽导致5'三磷酸暴露所致。U6 RNA的5'截断和TMG加帽似乎并不影响其在剪接中的正常功能,这表明剪接体的组装和作用对U6 RNA的5'端结构不是非常敏感。

相似文献

引用本文的文献

3
The life of U6 small nuclear RNA, from cradle to grave.U6 小核 RNA 的一生:从摇篮到坟墓。
RNA. 2018 Apr;24(4):437-460. doi: 10.1261/rna.065136.117. Epub 2018 Jan 24.

本文引用的文献

9
Architecture of a yeast U6 RNA gene promoter.酵母U6 RNA基因启动子的结构
Mol Cell Biol. 1993 May;13(5):3015-26. doi: 10.1128/mcb.13.5.3015-3026.1993.
10

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验