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首页> 外文期刊>Journal of Molecular Biology >Genetic interaction between yeast Saccharomyces cerevisiae release factorsand the decoding region of 18S rRNA
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Genetic interaction between yeast Saccharomyces cerevisiae release factorsand the decoding region of 18S rRNA

机译：酵母酿酒酵母释放因子与18S rRNA解码区之间的遗传相互作用

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Functional and structural similarities between tRNA and eukaryotic class 1 release factors (eRF1) described previously, provide evidence for the molecular mimicry concept. This concept is supported here by the demonstration of a genetic interaction between eRF1 and the decoding region of the ribosomal RNA, the site of tRNA-mRNA interaction. We show that the conditional lethality caused by a mutation in domain 1 of yeast eRF1 (P86A), that mimics the tRNA anticodon stem-loop, is rescued by compensatory mutations A1491G (rdn15) and U1495C (hyg1) in helix 44 of the decoding region and by U912C (rdn4) and G886A (rdn8) mutations in helix 27 of the 18 S rRNA. The udn15 mutation creates a C1409-G1491 base-pair in yeast rRNA that is analogous to that in prokaryotic rRNA known to be important for high-affinity paromomycin binding to the ribosome. indeed, rdn15 makes yeast cells extremely sensitive to paromomycin, indicating that the natural high resistance of the yeast ribosome to paromomycin is, in large part, due to the absence of the 1409-1491 base-pair. The rdn15 and hyg1 mutations also partially compensate for inactivation of the eukaryotic release factor 3 (eRF3) resulting from the formation of the [PSI+] prion, a self-reproducible termination-deficient conformation of eRF3. However, rdn15, but not hyg1, rescues the conditional cell lethality caused by a GTPase domain mutation (R419G) in eRF3. Other antisuppressor rRNA mutations, rdn2 (G517A), rdn1T(C1054T) and rdn12A(C526A), strongly inhibit [PSI (+)]-mediated stop codon read-through but do not cure cells of the [PSI (+)] prion. Interestingly, cells bearing hyg1 seem to enable [PSI (+)] strains to accumulate larger Sup35p aggregates upon Sup35p overproduction, suggesting a lower toxicity of overproduced Sup35p when the termination defect, caused by [PSI (+)], is partly relieved. (C) 2003 Academic Press.
机译：之前描述的tRNA与1类真核释放因子（eRF1）之间的功能和结构相似性，为分子模拟概念提供了证据。在此通过证明eRF1与核糖体RNA的解码区域（tRNA-mRNA相互作用的位点）之间的遗传相互作用来支持这一概念。我们显示，由酵母eRF1（P86A）的域1中的突变引起的条件致死性是由解码区域的螺旋44中的补偿性突变A1491G（rdn15）和U1495C（hyg1）挽救的，它模仿了tRNA反密码子茎环。以及18 S rRNA螺旋27中的U912C（rdn4）和G886A（rdn8）突变。 udn15突变在酵母rRNA中产生一个C1409-G1491碱基对，类似于已知对高亲和性巴龙霉素与核糖体结合很重要的原核rRNA中的碱基对。实际上，rdn15使酵母细胞对巴龙霉素极为敏感，这表明酵母核糖体对巴龙霉素的天然高抗性很大程度上是由于缺少1409-1491碱基对。 rdn15和hyg1突变还部分补偿了因[PSI +] ion病毒的形成而导致的真核生物释放因子3（eRF3）的失活，这是一种可自我复制的eRF3末端缺陷构象。但是，rdn15而非hyg1可以挽救eRF3中由GTPase域突变（R419G）引起的条件细胞杀伤力。其他抗抑制rRNA突变rdn2（G517A），rdn1T（C1054T）和rdn12A（C526A）强烈抑制[PSI（+）]介导的终止密码子通读，但不能治愈[PSI（+）] pr病毒的细胞。有趣的是，带有hyg1的细胞似乎在Sup35p过量生产时使[PSI（+）]菌株能够积累更大的Sup35p聚集体，这表明当由[PSI（+）]引起的终止缺陷被部分缓解时，过量生产的Sup35p的毒性较低。 （C）2003年学术出版社。

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