Petersen C
Institute of Microbiology, University of Copenhagen, Denmark.
J Mol Biol. 1989 Mar 20;206(2):323-32. doi: 10.1016/0022-2836(89)90482-8.
In Escherichia coli the genes encoding ribosomal proteins L10 and L7/L12, rplJ and rplL, are cotranscribed, and translation of both cistrons is regulated by binding of L10 or a complex of L10 and L7/L12 to a single target in the mRNA leader region. Co-ordinated regulation is assured by some kind of translational coupling, the mechanism of which was investigated here by deletion analysis of plasmids carrying either the intact rplL gene or rplL-lacZ gene fusions. Unless the rplL ribosome binding site was modified by deletion, efficient initiation of translation required translation of a region located more than 500 nucleotides upstream on the transcript within the rplJ cistron. It is proposed that the wild-type rplL ribosome binding site is blocked by long-range RNA base-pairing to this region, when translation of the rplJ sequence is inhibited.
在大肠杆菌中,编码核糖体蛋白L10和L7/L12的基因rplJ和rplL是共转录的,两个顺反子的翻译受L10或L10与L7/L12的复合物与mRNA前导区单个靶点的结合调控。通过某种翻译偶联确保协调调控,本文通过对携带完整rplL基因或rplL - lacZ基因融合体的质粒进行缺失分析来研究其机制。除非通过缺失修饰rplL核糖体结合位点,否则有效的翻译起始需要转录本上位于rplJ顺反子内上游超过500个核苷酸的区域进行翻译。有人提出,当rplJ序列的翻译受到抑制时,野生型rplL核糖体结合位点会被与该区域的长程RNA碱基配对所阻断。