Mitra Kakoli, Schaffitzel Christiane, Fabiola Felcy, Chapman Michael S, Ban Nenad, Frank Joachim
Howard Hughes Medical Institute, Health Research, Inc., at the Wadsworth Center, Empire State Plaza, Albany, New York 12201, USA.
Mol Cell. 2006 May 19;22(4):533-43. doi: 10.1016/j.molcel.2006.05.003.
In E. coli, the SecM nascent polypeptide causes elongation arrest, while interacting with 23S RNA bases A2058 and A749-753 in the exit tunnel of the large ribosomal subunit. We compared atomic models fitted by real-space refinement into cryo-electron microscopy reconstructions of a pretranslocational and SecM-stalled E. coli ribosome complex. A cascade of RNA rearrangements propagates from the exit tunnel throughout the large subunit, affecting intersubunit bridges and tRNA positions, which in turn reorient small subunit RNA elements. Elongation arrest could result from the inhibition of mRNA.(tRNAs) translocation, E site tRNA egress, and perhaps translation factor activation at the GTPase-associated center. Our study suggests that the specific secondary and tertiary arrangement of ribosomal RNA provides the basis for internal signal transduction within the ribosome. Thus, the ribosome may itself have the ability to regulate its progression through translation by modulating its structure and consequently its receptivity to activation by cofactors.
在大肠杆菌中，SecM新生多肽在与大核糖体亚基出口通道中的23S RNA碱基A2058和A749 - 753相互作用时会导致延伸停滞。我们比较了通过实空间精修拟合到预转位和SecM停滞的大肠杆菌核糖体复合物的冷冻电子显微镜重建模型中的原子模型。一系列RNA重排从出口通道传播到整个大亚基，影响亚基间桥和tRNA位置，进而使小亚基RNA元件重新定向。延伸停滞可能是由于mRNA（tRNAs）易位、E位点tRNA排出受到抑制，或许还有GTP酶相关中心处翻译因子激活受到抑制所致。我们的研究表明，核糖体RNA的特定二级和三级结构排列为核糖体内的内部信号转导提供了基础。因此，核糖体本身可能具有通过调节其结构从而调节其对辅因子激活的接受能力来调控其翻译进程的能力。
