Nakatogawa Hitoshi, Ito Koreaki
Institute for Virus Research and CREST, Japan Science and Technology Corporation, Kyoto University, Japan.
Cell. 2002 Mar 8;108(5):629-36. doi: 10.1016/s0092-8674(02)00649-9.
Translation of SecM stalls unless its N-terminal part is "pulled" by the protein export machinery. Here we show that the sequence motif FXXXXWIXXXXGIRAGP that includes a specific arrest point (Pro) causes elongation arrest within the ribosome. Mutations that bypass the elongation arrest were isolated in 23S rRNA and L22 r protein. Such suppressor mutations occurred at a few specific residues of these components, which all face the narrowest constriction of the ribosomal exit tunnel. Thus, we suggest that this region of the exit tunnel interacts with nascent translation products and functions as a discriminating gate.
SecM的翻译停滞,除非其N端部分被蛋白质输出机制“拉动”。我们在此表明,包含特定停滞点(脯氨酸)的序列基序FXXXXWIXXXXGIRAGP会导致核糖体内部的延伸停滞。在23S rRNA和L22核糖体蛋白中分离出了绕过延伸停滞的突变。此类抑制突变发生在这些组分的几个特定残基处,这些残基均面向核糖体出口通道最狭窄的缩窄处。因此,我们认为出口通道的这一区域与新生翻译产物相互作用,并作为一个识别门发挥作用。