Translational initiation frequency of atp genes from Escherichia coli: identification of an intercistronic sequence that enhances translation.
Translational initiation frequency of atp genes from Escherichia coli: identification of an intercistronic sequence that enhances translation.
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大肠杆菌 atp 基因的翻译起始频率：增强翻译的顺反子间序列的鉴定。
DOI：
10.1002/j.1460-2075.1985.tb03659.x
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发表时间：
1985
期刊：
影响因子：
--
通讯作者：
W. Sebald
中科院分区：
文献类型：
--
作者：
J. McCarthy;H. Schairer;W. Sebald
将大肠杆菌atp操纵子的c、B和δ亚基基因分别克隆到tac融合启动子和galK基因之间的表达载体中。由克隆基因指导的亚基合成的相对速率在体外和体内相似，并且与E.大肠杆菌中的表达。亚基c的合成速率至少是亚基B的6倍，是亚基δ的18倍。位于亚基c基因上游的长顺反子间序列的逐渐缩短表明，该基因的最大表达取决于Shine-Dalgarno位点上游延伸大于20 bp的序列的存在。因此，该序列起到提高翻译起始速率的作用。类似的序列可能在大肠杆菌的其他操纵子中执行相同的功能。大肠杆菌和λ噬菌体的研究进展。亚基B顺反子的翻译与前一个亚基c顺反子的翻译部分偶联。总之，所有atp操纵子基因的表达都可以调节，以适应ATP合酶组装的亚基要求，主要是通过控制各自顺反子起始密码子处翻译起始和再起始效率的机制。
The c, b and delta subunit genes of the Escherichia coli atp operon were cloned individually in an expression vector between the tac fusion promoter and the galK gene. The relative rates of subunit synthesis directed by the cloned genes were similar in vitro and in vivo and compared favourably with the subunit stoichiometry of the assembled proton‐translocating ATP synthase of E. coli in vivo. The rate of synthesis of subunit c was at least six times that of subunit b and 18 times that of subunit delta. Progressive shortening of the long intercistronic sequence lying upstream of the subunit c gene showed that maximal expression of this gene is dependent upon the presence of a sequence stretching greater than 20 bp upstream of the Shine‐Dalgarno site. This sequence thus acts to enhance the rate of translational initiation. The possibility that similar sequences might perform the same function in other operons of E. coli and bacteriophage lambda is also discussed. Translation of the subunit b cistron is partially coupled to translation of the preceding subunit c cistron. In conclusion, the expression of all the atp operon genes could be adjusted to accommodate the subunit requirements of ATP synthase assembly primarily by means of mechanisms which control the efficiency of translational initiation and re‐initiation at the respective cistron start codons.