Tait R C, Boyer H W
Cell. 1978 Jan;13(1):73-81. doi: 10.1016/0092-8674(78)90139-3.
In vitro enzymatic alteration of plasmid phenotype and in vitro construction of recombinant plasmids containing genetic information derived from the plasmid pSC101 have been used to investigate the mechanism of function of tetracycline resistance determined by the plasmid pSC101. The resistance has been shown to be inducible and involves the increased synthesis of membrane-associated polypeptides of 34,000, 26,000 and 14,000 daltons that are encoded for by the plasmid. The 34,000 dalton polypeptide along with another plasmid-encoded polypeptide of 18,000 daltons function in an ATP-independent manner to prevent the accumulation of tetracycline by the cell. These polypeptides are sufficient for resistance. A second component of plasmid-determined resistance involves the 14,000 dalton polypeptide and reduces the initial adsorption of tetracycline by sensitive cells, but is not alone sufficient for the generation of resistance. The role of the 26,000 dalton polypeptide in tetracycline resistance has not been identified.
利用体外对质粒表型的酶促改变以及体外构建含有源自质粒pSC101的遗传信息的重组质粒，来研究由质粒pSC101所决定的四环素抗性的功能机制。已表明这种抗性是可诱导的，并且涉及由该质粒编码的34000、26000和14000道尔顿的膜相关多肽合成增加。34000道尔顿的多肽与另一种18000道尔顿的质粒编码多肽以不依赖ATP的方式发挥作用，以防止细胞积累四环素。这些多肽足以产生抗性。质粒决定的抗性的第二个组成部分涉及14000道尔顿的多肽，它减少了敏感细胞对四环素的初始吸附，但单独不足以产生抗性。26000道尔顿的多肽在四环素抗性中的作用尚未明确。
