Brown S
Fred Hutchinson Cancer Research Center, Seattle, WA 98104.
J Mol Biol. 1989 Sep 5;209(1):79-90. doi: 10.1016/0022-2836(89)90171-x.
A new class of suppressor mutants helps to define the role of 4.5 S RNA in translation. The suppressors reduce the requirement for 4.5 S RNA by increasing the intracellular concentration of uncharged tRNA. Suppression probably occurs by prolonging the period in which translating ribosomes have translocated but not yet released the uncharged tRNA, indicating that this is the point at which 4.5 S RNA enters translation. The release of 4.5 S RNA from polysomes is affected by antibiotics that inhibit protein synthesis. The antibiotic-sensitivity of this release indicates that 4.5 S RNA exits the ribosome following translocation and prior to release of protein synthesis elongation factor G. These results indicate that 4.5 S RNA acts immediately after ribosomal translocation. A model is proposed in which 4.5 S RNA stabilizes the post-translocation state by replacing 23 S ribosomal RNA as a binding site for elongation factor G. The 4.5 S RNA-requirement of mutants altered in 23 S ribosomal RNA support this model.
一类新的抑制突变体有助于确定4.5S RNA在翻译中的作用。这些抑制突变体通过增加无电荷tRNA的细胞内浓度来降低对4.5S RNA的需求。抑制作用可能是通过延长翻译核糖体易位但尚未释放无电荷tRNA的时间段来发生的，这表明这是4.5S RNA进入翻译的点。4.5S RNA从多核糖体上的释放受到抑制蛋白质合成的抗生素的影响。这种释放的抗生素敏感性表明4.5S RNA在易位后且在蛋白质合成延伸因子G释放之前离开核糖体。这些结果表明4.5S RNA在核糖体易位后立即起作用。提出了一个模型，其中4.5S RNA通过取代23S核糖体RNA作为延伸因子G的结合位点来稳定易位后状态。23S核糖体RNA发生改变的突变体对4.5S RNA的需求支持了这一模型。
