Wegrzyn G, Glass R E, Thomas M S
Department of Biochemistry, University of Nottingham Medical School, Queen's Medical Centre, UK.
Gene. 1992 Dec 1;122(1):1-7. doi: 10.1016/0378-1119(92)90025-k.
Escherichia coli cells harbouring the rpoA341 mutation produce an RNA polymerase which transcribes inefficiently certain operons subject to positive control. Here, we demonstrate that the rpoA341 allele also prevents lysogenization of the host strain by bacteriophage lambda, a process dependent upon the action of two phage-encoded activators. This phenomenon was shown to arise from an inability to establish an integrated prophage rather than a failure to maintain the lysogenic state. The inability of the rpoA341 host to support lysogenization could be completely reversed by CII-independent expression of int and cI in trans. These results led us to propose that the inhibition of lysogenization arises from a defective interaction between the phage lambda transcriptional activator CII and the mutant RNA polymerase at the phage promoters pI and pE. Finally, we also provide genetic evidence for impaired transcription of the cI gene from the CI-activated promoter, pM in the rpoA341 background.
携带rpoA341突变的大肠杆菌细胞产生一种RNA聚合酶,该酶对某些受正调控的操纵子转录效率低下。在此,我们证明rpoA341等位基因也会阻止噬菌体λ对宿主菌株的溶原化,这一过程依赖于两种噬菌体编码激活因子的作用。这种现象被证明是由于无法建立整合的原噬菌体,而不是无法维持溶原状态。通过反式独立于CII表达int和cI,可以完全逆转rpoA341宿主支持溶原化的无能。这些结果使我们提出,溶原化的抑制源于噬菌体λ转录激活因子CII与突变RNA聚合酶在噬菌体启动子pI和pE处的缺陷相互作用。最后,我们还提供了遗传证据,证明在rpoA341背景下,从CI激活的启动子pM转录cI基因受损。