肽基转移酶活性降低与酿酒酵母中程序性-1核糖体移码增加及病毒维持缺陷相关。
Decreased peptidyltransferase activity correlates with increased programmed -1 ribosomal frameshifting and viral maintenance defects in the yeast Saccharomyces cerevisiae.
作者信息
Meskauskas Arturas, Harger Jason W, Jacobs Kristi L Muldoon, Dinman Jonathan D
机构信息
Department of Cell Biology and Molecular Genetics, University of Maryland, College Park, Maryland 20742, USA.
出版信息
RNA. 2003 Aug;9(8):982-92. doi: 10.1261/rna.2165803.
Abstract
Increased efficiencies of programmed -1 ribosomal frameshifting in yeast cells expressing mutant forms of ribosomal protein L3 are unable to maintain the dsRNA "Killer" virus. Here we demonstrate that changes in frameshifting and virus maintenance in these mutants correlates with decreased peptidyltransferase activities. The mutants did not affect Ty1-directed programmed +1 ribosomal frameshifting or nonsense-mediated mRNA decay. Independent experiments demonstrate similar programmed -1 ribosomal frameshifting specific defects in cells lacking ribosomal protein L41, which has previously been shown to result in peptidyltransferase defects in yeast. These findings are consistent with the hypothesis that decreased peptidyltransferase activity should result in longer ribosome pause times after the accommodation step of the elongation cycle, allowing more time for ribosomal slippage at programmed -1 ribosomal frameshift signals.
摘要
在表达核糖体蛋白L3突变形式的酵母细胞中，程序性-1核糖体移码效率的提高无法维持双链RNA“杀手”病毒。在这里，我们证明这些突变体中移码和病毒维持的变化与肽基转移酶活性降低相关。这些突变体不影响Ty1导向的程序性+1核糖体移码或无义介导的mRNA降解。独立实验表明，在缺乏核糖体蛋白L41的细胞中存在类似的程序性-1核糖体移码特异性缺陷，此前已证明该缺陷会导致酵母中的肽基转移酶缺陷。这些发现与以下假设一致：肽基转移酶活性降低应导致延伸循环容纳步骤后核糖体暂停时间延长，从而为程序性-1核糖体移码信号处的核糖体滑动留出更多时间。
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