PDF(Pubmed)
Abstract：
Plasmodium falciparum is a causative agent of human malaria. Sixty percent of mRNAs from its extremely AT-rich (81%) genome harbor long polyadenosine (polyA) runs within their ORFs, distinguishing the parasite from its hosts and other sequenced organisms. Recent studies indicate polyA runs cause ribosome stalling and frameshifting, triggering mRNA surveillance pathways and attenuating protein synthesis. Here, we show that P. falciparum is an exception to this rule. We demonstrate that both endogenous genes and reporter sequences containing long polyA runs are efficiently and accurately translated in P. falciparum cells. We show that polyA runs do not elicit any response from No Go Decay (NGD) or result in the production of frameshifted proteins. This is in stark contrast to what we observe in human cells or T. thermophila, an organism with similar AT-content. Finally, using stalling reporters we show that Plasmodium cells evolved not to have a fully functional NGD pathway.
摘要：
恶性疟原虫是人类疟疾的病原体。来自其富含AT（81％）基因组的60％的mRNA在其ORF中含有长的多腺苷（polyA），将寄生虫与其宿主和其他测序生物区分开来。最近的研究表明，polyA运行会导致核糖体停滞和移码，触发mRNA监测途径并减弱蛋白质合成。这里,我们证明恶性疟原虫是这一规则的例外。我们证明，内源性基因和含有长polyA运行的报告序列在恶性疟原虫细胞中都能有效和准确地翻译。我们表明，polyA运行不会引起NoGoDecay（NGD）的任何反应，也不会导致移码蛋白的产生。这与我们在人类细胞或嗜热菌中观察到的情况形成鲜明对比，具有相似AT含量的生物体。最后,使用停滞报告基因，我们发现疟原虫细胞进化到没有功能齐全的NGD途径。
