Jason L. Choy Laboratory of Single Molecule Biophysics and QB3 Institute, University of California, Berkeley, California 94720, USA.
Nature. 2011 Jul 6;475(7354):118-21. doi: 10.1038/nature10126.
The ribosome translates the genetic information encoded in messenger RNA into protein. Folded structures in the coding region of an mRNA represent a kinetic barrier that lowers the peptide elongation rate, as the ribosome must disrupt structures it encounters in the mRNA at its entry site to allow translocation to the next codon. Such structures are exploited by the cell to create diverse strategies for translation regulation, such as programmed frameshifting, the modulation of protein expression levels, ribosome localization and co-translational protein folding. Although strand separation activity is inherent to the ribosome, requiring no exogenous helicases, its mechanism is still unknown. Here, using a single-molecule optical tweezers assay on mRNA hairpins, we find that the translation rate of identical codons at the decoding centre is greatly influenced by the GC content of folded structures at the mRNA entry site. Furthermore, force applied to the ends of the hairpin to favour its unfolding significantly speeds translation. Quantitative analysis of the force dependence of its helicase activity reveals that the ribosome, unlike previously studied helicases, uses two distinct active mechanisms to unwind mRNA structure: it destabilizes the helical junction at the mRNA entry site by biasing its thermal fluctuations towards the open state, increasing the probability of the ribosome translocating unhindered; and it mechanically pulls apart the mRNA single strands of the closed junction during the conformational changes that accompany ribosome translocation. The second of these mechanisms ensures a minimal basal rate of translation in the cell; specialized, mechanically stable structures are required to stall the ribosome temporarily. Our results establish a quantitative mechanical basis for understanding the mechanism of regulation of the elongation rate of translation by structured mRNAs.
核糖体将信使 RNA 中编码的遗传信息翻译成蛋白质。mRNA 编码区的折叠结构代表了一个动力学障碍,降低了肽延伸的速度,因为核糖体必须破坏其在 mRNA 进入位点遇到的结构,以允许向下一个密码子易位。这些结构被细胞用来创造多样化的翻译调控策略,如程序性移码、蛋白质表达水平的调节、核糖体定位和共翻译蛋白质折叠。尽管核糖体本身具有链分离活性,不需要外源解旋酶,但它的机制仍不清楚。在这里,我们使用单个分子光学镊子测定法研究 mRNA 发夹,发现翻译中心相同密码子的翻译速度受到 mRNA 进入位点折叠结构的 GC 含量的极大影响。此外,对发夹末端施加力以促进其展开,可显著加快翻译速度。对其解旋酶活性的力依赖性的定量分析表明,核糖体与之前研究的解旋酶不同,它使用两种不同的活性机制来解开 mRNA 结构:它通过使 mRNA 进入位点的螺旋结不稳定,使热波动偏向开放状态,从而增加核糖体无障碍易位的概率;并且它在伴随核糖体易位的构象变化期间,机械地拉开封闭结的 mRNA 单链。后一种机制确保了细胞中最小的基础翻译速率;需要专门的、机械稳定的结构来暂时使核糖体停顿。我们的结果为理解结构 mRNA 对翻译延伸速度的调控机制提供了定量的力学基础。