Lamont I, Brumby A M, Egan J B
Department of Biochemistry, University of Adelaide, Australia.
Proc Natl Acad Sci U S A. 1989 Jul;86(14):5492-6. doi: 10.1073/pnas.86.14.5492.
Our results show that UV induction of the 186 prophage depends upon the phage function Tum, with the mutant phenotype of turbid plaques on mitomycin plates and the expression of which is controlled by the host LexA protein. Tum function, encoded near the right-hand end of the coliphage 186 chromosome, is under the control of promoter p95. This promoter is overlapped by a sequence closely related to the consensus sequence of the LexA-binding site. It is proposed that inactivation of LexA after UV irradiation (or by genetic means) leads to prophage induction by permitting expression of Tum which, by unknown means, induces prophage. This mechanism is basically different from that seen with the UV-inducible lambdoid coliphages, which are not regulated by LexA.
我们的结果表明,186原噬菌体的紫外线诱导依赖于噬菌体功能Tum,其在丝裂霉素平板上具有浑浊噬菌斑的突变表型,且其表达受宿主LexA蛋白控制。Tum功能由大肠杆菌噬菌体186染色体右手端附近编码,受启动子p95控制。该启动子与LexA结合位点的共有序列密切相关的序列重叠。有人提出,紫外线照射后(或通过遗传手段)LexA失活,通过允许Tum表达导致原噬菌体诱导,而Tum通过未知方式诱导原噬菌体。这种机制与紫外线诱导的类λ大肠杆菌噬菌体的机制基本不同,后者不受LexA调控。