Strauch M A, Baumann M, Friedman D I, Baron L S
J Bacteriol. 1986 Jul;167(1):191-200. doi: 10.1128/jb.167.1.191-200.1986.
Mutations in two Escherichia coli genes, sipA and sipB, result in a specific inhibition of the growth of certain hybrid lambdoid bacteriophages, lambda immP22, that have the early regulatory regions and adjacent genes from bacteriophage P22. The sipB391 mutation maps near minute 56 and exerts the strongest inhibitory effect on the growth of the hybrid phages. The sipA1 mutation maps near minute 72 and plays an auxiliary role: enhancing the action of sipB391. Such a role is not limited to sipA1, since there is a similar enhancement by the nusA1 and nusE71 mutations. The Sip-imposed restriction on the growth of lambda immP22 phages is not observed if the phage carries a mutation in the c1 gene. Perhaps this reflects the fact that the c1 product regulates phage DNA replication and is a major determinant in the decision governing whether the phage takes the lytic or lysogenic pathway. Consistent with this idea is the observation that lambda immP22 DNA replication is severely inhibited in bacteria carrying the sipB391 mutation. It is suggested that sip mutations exaggerate the normal role of c1 in limiting lytic growth. This causes a failure in the expression of sufficient amounts of some or all of the lytic gene products required for phage growth.
大肠杆菌的两个基因sipA和sipB发生突变,会导致某些具有噬菌体P22早期调控区域及相邻基因的杂合λ样噬菌体(λimmP22)的生长受到特异性抑制。sipB391突变位于56分钟附近,对杂合噬菌体的生长具有最强的抑制作用。sipA1突变位于72分钟附近,起辅助作用:增强sipB391的作用。这种作用不限于sipA1,因为nusA1和nusE71突变也有类似的增强作用。如果噬菌体的c1基因发生突变,则不会观察到Sip对λimmP22噬菌体生长的限制作用。这可能反映了这样一个事实,即c1产物调节噬菌体DNA复制,并且是决定噬菌体采取裂解或溶原途径的主要决定因素。与这一观点一致的是,在携带sipB391突变的细菌中,λimmP22 DNA复制受到严重抑制。有人提出,sip突变夸大了c1在限制裂解生长中的正常作用。这导致无法表达噬菌体生长所需的足够数量的部分或全部裂解基因产物。