Fitts R A, Taylor A L
Proc Natl Acad Sci U S A. 1980 May;77(5):2801-5. doi: 10.1073/pnas.77.5.2801.
The target site for bacteriophage Mu integration in a lytic cycle of infection was investigated. DNA synthesis in five Hfr strains of Escherichia coli K-12 was synchronized by amino acid starvation and was allowed to proceed for 0, 8, or 15 min before infection. The Hfr cells were then infected with Mu and were subsequently mated with nonimmune F- recipient cells. Mating was interrupted mechanically at 5-min intervals and samples were assayed for infective centers. Conjugal transfer of Mu was delayed in Hfr strains that have transfer origins 15 map units or more from the E. coli replication origin, and the delays increased as the distance between an Hfr point of origin and the replication origin increased. When a gene A mutant of Mu was used for the infection, no infective centers were generated. Infection with a gene B mutant resulted in infective center formation only after long periods of mating. These data are most consistent with a model in which infecting Mu DNA or its progeny integrate at host chromosomal replication forks.
研究了噬菌体Mu在裂解性感染周期中的整合靶位点。通过氨基酸饥饿使5株大肠杆菌K - 12的Hfr菌株中的DNA合成同步化，并在感染前分别进行0、8或15分钟的DNA合成。然后用Mu感染Hfr细胞，随后将其与非免疫F -受体细胞进行交配。每隔5分钟机械中断交配，并对样品进行感染中心检测。在转移起点距大肠杆菌复制起点15个或更多图距单位的Hfr菌株中，Mu的接合转移延迟，并且随着Hfr起点与复制起点之间距离的增加，延迟时间也增加。当使用Mu的基因A突变体进行感染时，未产生感染中心。用基因B突变体感染仅在长时间交配后才导致感染中心形成。这些数据与一个模型最为一致，即感染的Mu DNA或其后代在宿主染色体复制叉处整合。
