Jones I M, Primrose S B, Robinson A, Ellwood D C
Mol Gen Genet. 1980;180(3):579-84. doi: 10.1007/BF00268063.
When cells carrying the plasmids RP1, pDS4101 (a ColK derivative) or pDS1109 (a ColE1 derivative) were maintained in chemostat culture in the absence of antibiotic selection, plasmid-free segregants were not detected after 120 generations of nutrient-limited growth. By contrast, plasmid-free segregants of pMB9- and pBR322-containing cells arose after approximately 30 generations, irrespective of the host genetic background. However, even though pDS1109 was maintained its copy-number fell five-fold during 80 generations of limited growth. It is suggested that loss of pBR322 occurs following a similar copy-number decrease which results in defective segregation of the plasmid to daughter host cells. This defective segregation was not complemented in trans by either RP1 or pDS4101.
当携带质粒RP1、pDS4101(一种ColK衍生物)或pDS1109(一种ColE1衍生物)的细胞在无抗生素选择的情况下进行恒化培养时,在营养受限生长120代后未检测到无质粒的分离菌。相比之下,无论宿主遗传背景如何,含有pMB9和pBR322的细胞的无质粒分离菌在大约30代后出现。然而,尽管pDS1109得以维持,但其拷贝数在80代的有限生长过程中下降了五倍。有人提出,pBR322的丢失是在类似的拷贝数减少之后发生的,这导致质粒向子代宿主细胞的分离出现缺陷。这种有缺陷的分离不能被RP1或pDS4101反式互补。