Genetic interactions between [PSI+] and nonstop mRNA decay affect phenotypic variation.
Genetic interactions between [PSI+] and nonstop mRNA decay affect phenotypic variation.
复制标题
[PSI] 和不间断 mRNA 衰减之间的遗传相互作用会影响表型变异。
DOI：
10.1073/pnas.0504557102
复制
发表时间：
2005
影响因子：
11.1
通讯作者：
vanHoof,Ambro
中科院分区：
文献类型：
--
作者：
Wilson,MarendaA;Meaux,Stacie;Parker,Roy;vanHoof,Ambro
酵母菌株可以在[PSI+]和[psi-]状态之间可逆地相互转化。[PSI+]状态是由翻译终止因子eRF 3的朊病毒形式引起的。[PSI+]状态导致在终止密码子处的通读，并且可以导致表型变异，尽管引起这些表型变化的分子机制仍然未知。我们确定了[PSI+]诱导的表型变异和不间断mRNA衰减缺陷之间的相互作用。当核糖体到达转录物的3′端时，会触发mRNA的不间断衰变。相反，我们观察到[PSI+]诱导的表型变异和无义介导的衰变缺陷之间几乎没有相互作用，这导致过早终止密码子的抑制。这些结果表明，[PSI+]的至少一些表型效应可能是由于“正常”终止密码子的通读，从而产生延伸蛋白。此外，这些观察结果表明，不间断的mRNA衰减可能会限制[PSI+]诱导的表型变异。这样的过程将允许对3′ UTR进行周期性取样，其可以快速发散，用于新的和有益的蛋白质延伸。
Yeast strains can reversibly interconvert between [PSI+] and [psi-] states. The [PSI+] state is caused by a prion form of the translation termination factor eRF3. The [PSI+] state causes read-through at stop codons and can lead to phenotypic variation, although the molecular mechanisms causing those phenotypic changes remain unknown. We identify an interaction between [PSI+]-induced phenotypic variation and defects in nonstop mRNA decay. Nonstop mRNA decay is triggered when a ribosome reaches the 3′ end of the transcript. In contrast, we observed little interaction between [PSI+]-induced phenotypic variation and defects in nonsense-mediated decay, which lead to suppression of premature stop codons. These results suggest that at least some of the phenotypic effects of [PSI+] may be due to read-through of “normal” stop codons, thereby producing extended proteins. Moreover, these observations suggest that nonstop mRNA decay may limit [PSI+]-induced phenotypic variation. Such a process would allow periodic sampling of the 3′ UTR, which can diverge rapidly, for novel and beneficial protein extensions.