Nagata T, Murakami Y, Imai M
Institute for Virus Research, Kyoto University, Japan.
Mol Gen Genet. 1988 Jul;213(1):163-5. doi: 10.1007/BF00333414.
The phenotype of Escherichia coli dnaA missense and nonsense mutations was integratively suppressed by plasmid R100-1. The suppressed strains, however, could not survive when the dnaA function was totally inactivated. This was demonstrated by the inability of replacing the dnaA allele in the suppressed strain by a dnaA::Tn10 insertion using phage P1-mediated transduction. When the intact dnaA+ allele was additionally supplied by a specialized transducing phage, lambda imm21 dnaA+, which integrated at the att lambda site on the E. coli chromosome, then the dnaA::Tn10 insertion, together with a delta oriC deletion, were able to be introduced into the suppressed strain. Thus, the mechanisms of dnaA function for oriC and for the replication origin of R100-1 may not be quite the same.
大肠杆菌dnaA错义突变和无义突变的表型被质粒R100-1整合抑制。然而,当dnaA功能完全失活时,被抑制的菌株无法存活。这通过使用噬菌体P1介导的转导无法用dnaA::Tn10插入取代被抑制菌株中的dnaA等位基因得以证明。当完整的dnaA+等位基因由专门的转导噬菌体λimm21 dnaA+额外提供时,该噬菌体整合在大肠杆菌染色体的attλ位点上,那么dnaA::Tn10插入以及oriC缺失能够被引入被抑制的菌株中。因此,dnaA对oriC和R100-1复制起点的功能机制可能并不完全相同。