Yarmolinsky M B, Stevens E
Mol Gen Genet. 1983;192(1-2):140-8. doi: 10.1007/BF00327659.
UV-damaged bacteriophage P1 causes an SOS response in infected bacteria that can be measured colorimetrically with the aid of a lambda pL-lacZ fusion strain of Escherichia coli. This response is blocked by a P1 prophage. Evidence is offered that the blockage is caused by the concerted action of the incompatibility determinant incA and the immunity (c1 and c4) repressors of the prophage. We suggest that indirect induction of lambda by damaged P1 is caused by the abortive initiation of replication in either of two modes, one under incA control, the other under c1 control and indirectly (via ant, the determinant of a repression antagonist) under c4 control.
紫外线损伤的噬菌体P1会在受感染细菌中引发SOS反应，借助大肠杆菌的λ pL - lacZ融合菌株，可通过比色法对该反应进行测定。这种反应会被P1原噬菌体阻断。有证据表明，这种阻断是由不相容性决定因子incA与原噬菌体的免疫（c1和c4）阻遏物协同作用所致。我们认为，受损的P1对λ的间接诱导是由两种复制起始模式之一的流产性起始引起的，一种受incA控制，另一种受c1控制，还有一种通过c4控制下的间接方式（通过阻遏拮抗剂的决定因子ant）。
