DEG1, encoding the tRNA:pseudouridine synthase Pus3p, impacts HOT1-stimulated recombination in Saccharomyces cerevisiae.
DEG1, encoding the tRNA:pseudouridine synthase Pus3p, impacts HOT1-stimulated recombination in Saccharomyces cerevisiae.
复制标题
DEG1 编码 tRNA：假尿苷合酶 Pus3p，影响酿酒酵母中 HOT1 刺激的重组。
DOI：
10.1007/s00438-005-0042-3
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发表时间：
2005
期刊：
影响因子：
--
通讯作者：
Keil,RL
中科院分区：
文献类型：
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作者：
Hepfer,CE;Arnold-Croop,S;Fogell,H;Steudel,KG;Moon,M;Roff,A;Zaikoski,S;Rickman,A;Komsisky,K;Harbaugh,DL;Lang,GI;Keil,RL
在酿酒酵母中，hot1刺激的重组与维持重复核糖体RNA基因之间的同源性有关。hot1刺激基因交换的能力需要RNA聚合酶I在重组序列上的转录。反式作用核突变hrm3-1特异性地减少hot1依赖性重组，并在37°时阻止细胞生长。hr3基因与deg1相同。在hot1相邻序列indeg1Δ突变体中，重组减少，但不是基因替代。基因组rDNA重复序列内的精确重组也减少了。低重组和温度敏感表型ofdeg1Δ突变体是隐性的。deg1的缺失不影响hot1或rDNA的转录率，这表明转录是hot1活性的必要条件，但不是充分条件。伪尿嘧啶合成酶3 （Pus3p）是deg1基因的产物，通过催化尿嘧啶转化为伪尿嘧啶，修饰转运RNA的38和39位反密码子臂。缺乏假尿嘧啶合成酶编码的byPUS1、pus2或pus4的细胞没有表现出重组缺陷，表明Pus3p在hot1活性中起特定作用。Pus3p在翻译过程中调节帧移和读透事件的能力是独一无二的，其活性的这一方面可能是在突变体中观察到的hot1重组表型的原因。
InSaccharomyces cerevisiae,HOT1-stimulated recombination has been implicated in maintaining homology between repeated ribosomal RNA genes. The ability ofHOT1to stimulate genetic exchange requires RNA polymerase I transcription across the recombining sequences. Thetrans-acting nuclear mutationhrm3-1specifically reducesHOT1-dependent recombination and prevents cell growth at 37°. TheHRM3gene is identical toDEG1. Excisive, but not gene replacement, recombination is reduced inHOT1-adjacent sequences indeg1Δ mutants. Excisive recombination within the genomic rDNA repeats is also decreased. The hypo-recombination and temperature-sensitive phenotypes ofdeg1Δ mutants are recessive. Deletion ofDEG1did not affect the rate of transcription fromHOT1or rDNA suggesting that while transcription is necessary it is not sufficient forHOT1activity. Pseudouridine synthase 3 (Pus3p), theDEG1gene product, modifies the anticodon arm of transfer RNA at positions 38 and 39 by catalyzing the conversion of uridine to pseudouridine. Cells deficient in pseudouridine synthases encoded byPUS1, PUS2orPUS4displayed no recombination defects, indicating that Pus3p plays a specific role inHOT1activity. Pus3p is unique in its ability to modulate frameshifting and readthrough events during translation, and this aspect of its activity may be responsible forHOT1recombination phenotypes observed indeg1mutants.