Light J, Baumberg S
Mol Gen Genet. 1983;189(2):309-13. doi: 10.1007/BF00337822.
Previous results (Baumberg and Lovett 1977) showed that many conjugative plasmids, most notably those of the IncFII group, were only transferable to Escherichia coli K12 rho mutants at very low frequencies, and that this appeared to be due to a lethal interaction between plasmid and rho- allele. Experiments reported here were designed to examine this phenomenon further, and in particular to test the possibility that uncontrolled plasmid replication in the presence of the rho mutant allele occurs. The rifampicin resistance allele rpo203 antagonizes the effect of rho201 on conjugal plasmid transfer; since the former is known to counteract the latter's effect on transcription termination, this result indicates that the plasmid-rho interaction stems directly from the lack of transcription termination caused by a rho mutant allele. Direct estimation of Rldrd19 replication after conjugal transfer to rho+ and rho201 recipients showed no difference according to rho status. Also, cotransduction of rho101 and 201 with ilv::Tn5 into recipients carrying miniplasmid derivatives of R1, which retain a restriction fragment containing all the DNA known to be involved in plasmid replication, was normal and the rho- transductants retained the miniplasmids. It therefore appears that the lethal interaction between the Inc FII plasmids and rho mutant alleles does not involve plasmid replication functions.
先前的结果（鲍姆贝格和洛维特，1977年）表明，许多接合质粒，尤其是那些IncFII组的质粒，仅能以极低的频率转移到大肠杆菌K12 rho突变体中，而且这似乎是由于质粒与rho等位基因之间的致死性相互作用所致。本文报道的实验旨在进一步研究这一现象，特别是测试在rho突变等位基因存在的情况下发生不受控制的质粒复制的可能性。利福平抗性等位基因rpo203可拮抗rho201对接合质粒转移的影响；由于已知前者可抵消后者对转录终止的影响，这一结果表明质粒与rho的相互作用直接源于rho突变等位基因导致的转录终止缺失。对Rldrd19在接合转移至rho+和rho201受体后复制情况的直接估计显示，根据rho状态并无差异。此外，将rho101和201与ilv::Tn5共转导至携带R1微型质粒衍生物的受体中，该衍生物保留了一个包含所有已知参与质粒复制的DNA的限制片段，结果正常，且rho -转导子保留了微型质粒。因此，Inc FII质粒与rho突变等位基因之间的致死性相互作用似乎并不涉及质粒复制功能。
