Miyajima A, Yokota T, Takebe Y, Nakamura M, Kaziro Y
J Biochem. 1983 Apr;93(4):1101-8. doi: 10.1093/oxfordjournals.jbchem.a134235.
Of the two plasmids pTUB1 and pTUB2 constructed by cloning of the 8.9 kb EcoRI fragment carrying tufB (Miyajima, A., Shibuya, M., & Kaziro, Y. (1979) FEBS Lett. 102, 207-210), pTUB2 possesses a deletion of about 0.3 kb. Restriction and sequence analyses have located the deletion in the region of the four tRNA genes thrU-tyrU-glyT-thrT upstream of the tufB structural gene. As a result of homologous recombination between thrU and thrT, the four tRNA genes have been replaced by a single thrU-thrT hybrid gene. The deletion of the three tRNA genes does not significantly alter the in vivo expression of tufB as assessed by the kirromycin-sensitive phenotype of the transformant cells and by the synthesis of EF-Tu in mini-cells. Nor does the deletion affect the synthesis of beta-galactosidase in lysogens carrying a lambda transducing phage with a tufB-lacZ fusion. Transcription of tufB and synthesis of EF-Tu in a cell-free transcription-translation coupled system were essentially the same, regardless of whether pTUB1 or pTUB2 DNA was used as a template. Likewise, 0.2 mM ppGpp inhibits the synthesis of tufB mRNA on both pTUB1 and pTUB2 templates to the same extent. We concluded that the replacement by thrU-thrT hybrid gene of the four tRNA genes upstream of the tufB coding region does not significantly affect either in vivo or in vitro expression of tufB.
通过克隆携带tufB的8.9 kb EcoRI片段构建的两个质粒pTUB1和pTUB2(宫岛,A.,涩谷,M.,& 神代,Y.(1979年)《欧洲生物化学学会联合会快报》102,207 - 210)中,pTUB2有大约0.3 kb的缺失。限制性内切酶分析和序列分析已确定该缺失位于tufB结构基因上游的四个tRNA基因thrU - tyrU - glyT - thrT区域。由于thrU和thrT之间的同源重组,四个tRNA基因已被一个单一的thrU - thrT杂交基因所取代。通过转化细胞对奇霉素敏感的表型以及在小细胞中EF - Tu的合成来评估,三个tRNA基因的缺失并未显著改变tufB在体内的表达。该缺失也不影响携带带有tufB - lacZ融合的λ转导噬菌体的溶源菌中β - 半乳糖苷酶的合成。无论使用pTUB1还是pTUB2 DNA作为模板,在无细胞转录 - 翻译偶联系统中tufB的转录和EF - Tu的合成基本相同。同样,0.2 mM的ppGpp对pTUB1和pTUB2模板上tufB mRNA合成的抑制程度相同。我们得出结论,tufB编码区上游的四个tRNA基因被thrU - thrT杂交基因取代,并不会显著影响tufB在体内或体外的表达。