Basic Sciences Division and Computational Biology Program of the Public Health Sciences Division, Fred Hutchinson Cancer Center, Seattle, Washington, United States of America.
Biological Physics, Structure and Design Graduate Program, University of Washington, Seattle, Washington, United States of America.
PLoS Genet. 2022 Oct 31;18(10):e1010460. doi: 10.1371/journal.pgen.1010460. eCollection 2022 Oct.
Upstream open reading frames (uORFs) are present in over half of all human mRNAs. uORFs can potently regulate the translation of downstream open reading frames through several mechanisms: siphoning away scanning ribosomes, regulating re-initiation, and allowing interactions between scanning and elongating ribosomes. However, the consequences of these different mechanisms for the regulation of protein expression remain incompletely understood. Here, we performed systematic measurements on the uORF-containing 5' UTR of the cytomegaloviral UL4 mRNA to test alternative models of uORF-mediated regulation in human cells. We find that a terminal diproline-dependent elongating ribosome stall in the UL4 uORF prevents decreases in main ORF protein expression when ribosome loading onto the mRNA is reduced. This uORF-mediated buffering is insensitive to the location of the ribosome stall along the uORF. Computational kinetic modeling based on our measurements suggests that scanning ribosomes dissociate rather than queue when they collide with stalled elongating ribosomes within the UL4 uORF. We identify several human uORFs that repress main ORF protein expression via a similar terminal diproline motif. We propose that ribosome stalls in uORFs provide a general mechanism for buffering against reductions in main ORF translation during stress and developmental transitions.
上游开放阅读框(uORFs)存在于超过一半的人类 mRNA 中。uORFs 可以通过几种机制强烈调节下游开放阅读框的翻译:虹吸扫描核糖体、调节重新起始、以及允许扫描核糖体和延伸核糖体之间的相互作用。然而,这些不同机制对蛋白质表达调节的后果仍不完全了解。在这里,我们对巨细胞病毒 UL4 mRNA 中含有 uORF 的 5'UTR 进行了系统测量,以测试人类细胞中 uORF 介导的调节的替代模型。我们发现,UL4 uORF 中末端二脯氨酸依赖性延伸核糖体停滞可防止当 mRNA 上的核糖体加载减少时主 ORF 蛋白表达的降低。这种 uORF 介导的缓冲对核糖体停滞在 uORF 中的位置不敏感。基于我们的测量结果的计算动力学建模表明,当扫描核糖体在 UL4 uORF 内与停滞的延伸核糖体碰撞时,它们会解离而不是排队。我们鉴定了几个通过类似末端二脯氨酸基序抑制主 ORF 蛋白表达的人类 uORFs。我们提出,uORF 中的核糖体停滞为在应激和发育过渡期间缓冲主 ORF 翻译减少提供了一种通用机制。