Astrachan L, Miller J F
J Virol. 1972 Mar;9(3):510-8. doi: 10.1128/JVI.9.3.510-518.1972.
The ability of Escherichia coli K to support bacteriophage T4rII replication starts to decline at 3 to 6 min after infection by lambda. This inhibition appears to depend on expression of the lambdarex(+) gene, since little inhibition was observed following infection by a lambdarex mutant or by a hybrid bacteriophage lambdai(434) which lacks a functional rex gene. For promotion of the synthesis of rex product, cII(+) and N(+) genes are required and can act trans, whereas cY(+), also required, must be cis to a rex(+) gene. These genes presumably play a role in the transcription of the cI-rex operon because they are also known to be required for repressor (cI product) synthesis. Functional cIII, O, P genes are not necessary for ample rex product synthesis. We also observed full rex expression after infection by lambdasuscI mutants, suggesting that rex and repressor are separate gene products and that repressor is not required for inhibition of T4rII replication. We also report experiments with a rex mutant that is not leaky when in a lysogen but is sufficiently leaky shortly after infection to cause inhibition of T4rII replication.
大肠杆菌K支持噬菌体T4rII复制的能力在被λ噬菌体感染后3至6分钟开始下降。这种抑制作用似乎取决于λrex(+)基因的表达,因为在用λrex突变体或缺乏功能性rex基因的杂交噬菌体λi(434)感染后,几乎未观察到抑制作用。为促进rex产物的合成,需要cII(+)和N(+)基因,它们可以反式作用,而同样需要的cY(+)必须与rex(+)基因顺式排列。这些基因可能在cI-rex操纵子的转录中起作用,因为已知它们也是阻遏物(cI产物)合成所必需的。功能性的cIII、O、P基因对于充足的rex产物合成不是必需的。我们还观察到在用λsus cI突变体感染后有完全的rex表达,这表明rex和阻遏物是不同的基因产物,并且阻遏物对于抑制T4rII复制不是必需的。我们还报告了用一个rex突变体进行的实验,该突变体在溶原状态下不渗漏,但在感染后不久足够渗漏以导致T4rII复制受到抑制。