Rex1p deficiency leads to accumulation of precursor initiator tRNAMet and polyadenylation of substrate RNAs in Saccharomyces cerevisiae.
Rex1p deficiency leads to accumulation of precursor initiator tRNAMet and polyadenylation of substrate RNAs in Saccharomyces cerevisiae.
复制标题
DOI：
10.1093/nar/gkn925
复制
发表时间：
2009-01
影响因子：
14.9
通讯作者：
Anderson JT
中科院分区：
文献类型：
--
作者：
Ozanick SG;Wang X;Costanzo M;Brost RL;Boone C;Anderson JT
一个合成的基因阵列被用来鉴定当编码tRNA修饰酶亚基的TRM6的突变与酿酒酵母中任何非必需基因的缺失相结合时产生的致死和生长缓慢的表型。我们发现REx1基因的缺失导致了trm6-504菌株的生长缓慢。以前，REx1被证明参与处理5S rRNA的3‘端和二聚体tRNAArg-tRNAAsp。在本研究中，我们发现了在加工tRNAiMet前体的3‘端时需要Rex1p，并表明前体tRNAiMet在Trm6-504Rex1Δ菌株中积累。Rex1p的缺失导致其底物(包括tRNAiMet)的多聚腺苷化，表明3‘端加工缺陷可以激活核监视途径。最后，纯化的Rex1p在体外表现出依赖于镁离子的核糖核酸酶活性，该酶被两个高度保守的氨基酸突变失活。
A synthetic genetic array was used to identify lethal and slow-growth phenotypes produced when a mutation in TRM6, which encodes a tRNA modification enzyme subunit, was combined with the deletion of any non-essential gene in Saccharomyces cerevisiae. We found that deletion of the REX1 gene resulted in a slow-growth phenotype in the trm6-504 strain. Previously, REX1 was shown to be involved in processing the 3′ ends of 5S rRNA and the dimeric tRNAArg-tRNAAsp. In this study, we have discovered a requirement for Rex1p in processing the 3′ end of tRNAiMet precursors and show that precursor tRNAiMet accumulates in a trm6-504 rex1Δ strain. Loss of Rex1p results in polyadenylation of its substrates, including tRNAiMet, suggesting that defects in 3′ end processing can activate the nuclear surveillance pathway. Finally, purified Rex1p displays Mg2+-dependent ribonuclease activity in vitro, and the enzyme is inactivated by mutation of two highly conserved amino acids.
登录
查看更多内容
影响因子：
--
作者：
Chen, Y;Beck, A;Tavtigian, SV
通讯作者：
Tavtigian, SV
影响因子：
4.5
作者：
Kufel, J;Tollervey, D
通讯作者：
Tollervey, D
DOI：
10.1006/bbrc.1998.9664
发表时间：
1998-11-18
影响因子：
3.1
作者：
Moreno, JMP;Kildsgaard, J;Sperling-Petersen, HU
通讯作者：
Sperling-Petersen, HU
影响因子：
4.8
作者：
Braglia, P;Percudani, R;Dieci, G
通讯作者：
Dieci, G
影响因子：
3.2
作者：
ITO, H;FUKUDA, Y;KIMURA, A
通讯作者：
KIMURA, A