Suzuki T, Terasaki M, Takemoto-Hori C, Hanada T, Ueda T, Wada A, Watanabe K
Department of Integrated Biosciences, Graduate School of Frontier Sciences, University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113-8656, Japan.
J Biol Chem. 2001 Jun 15;276(24):21724-36. doi: 10.1074/jbc.M100432200. Epub 2001 Feb 21.
The mammalian mitochondrial ribosome (mitoribosome) is a highly protein-rich particle in which almost half of the rRNA contained in the bacterial ribosome is replaced with proteins. It is known that mitochondrial translation factors can function on both mitochondrial and Escherichia coli ribosomes, indicating that protein components in the mitoribosome compensate the reduced rRNA chain to make a bacteria-type ribosome. To elucidate the molecular basis of this compensation, we analyzed bovine mitoribosomal large subunit proteins; 31 proteins were identified including 15 newly identified proteins with their cDNA sequences from human and mouse. The results showed that the proteins with binding sites on rRNA shortened or lost in the mitoribosome were enlarged when compared with the E. coli counterparts; this suggests the structural compensation of the rRNA deficit by the enlarged proteins in the mitoribosome.
哺乳动物线粒体核糖体（线粒体核糖体）是一种蛋白质高度丰富的颗粒，其中细菌核糖体中所含的几乎一半rRNA被蛋白质所取代。已知线粒体翻译因子可在线粒体核糖体和大肠杆菌核糖体上发挥作用，这表明线粒体核糖体中的蛋白质成分补偿了缩短的rRNA链，从而形成了细菌型核糖体。为了阐明这种补偿的分子基础，我们分析了牛线粒体核糖体大亚基蛋白；共鉴定出31种蛋白质，其中包括15种新鉴定的蛋白质，其cDNA序列来自人类和小鼠。结果表明，与大肠杆菌对应物相比，在线粒体核糖体中rRNA上结合位点缩短或缺失的蛋白质有所增大；这表明线粒体核糖体中增大的蛋白质对rRNA缺陷进行了结构补偿。
