Yu A, Bertani L E, Haggård-Ljungquist E
Department of Microbial Genetics, Karolinska Institutet, Stockholm, Sweden.
Gene. 1989 Aug 1;80(1):1-11. doi: 10.1016/0378-1119(89)90244-8.
Integration of bacteriophage P2 into the Escherichia coli host genome involves recombination between two specific attachment sites, attP and attB, one on the phage and the other on the host genome, respectively. The reaction is controlled by the product of the phage int gene, a basic polypeptide of about 37 kDa [Ljungquist and Bertani, Mol. Gen. Genet. 192 (1983) 87-94]. The int gene appears to be expressed differently by an infecting phage, as opposed to a prophage [Bertani, Proc. Natl. Acad. Sci. USA 65 (1970) 331-336]. A 1200-bp region of P2 DNA containing the int gene and attP, the prophage hybrid ends attL and attR, and one bacterial attachment site, the preferred site locI from E. coli strain C, have all been sequenced. An open reading frame coding for a polypeptide of 337 amino acids corresponds to the int gene. The gene has no obvious promoter sequence preceding it. The int gene transcript seems to continue past the attP site downstream from it, suggesting a possible explanation for the previously observed difference in integration and excision. A comparison of the four attachment sites reveals a common 'core' sequence of 27 bp: 5'-AAAAAATAAGCCCGTGTAAGGGAGATT-3'. The P2 nip1 mutation, which increases prophage excision [Calendar et al., Virology 47 (1972) 68-75], was found to lie within the int gene itself. The P2 saf variant, which has altered site preference [Six, Virology 29 (1966) 106-125], has a bp substitution within the core sequence. Three deletion/substitution mutants, vir22, vir94 and del3, also have altered core sequences.
噬菌体P2整合到大肠杆菌宿主基因组中涉及两个特定附着位点attP和attB之间的重组,其中attP位于噬菌体上,attB则位于宿主基因组上。该反应由噬菌体int基因的产物控制,int基因产物是一种约37 kDa的碱性多肽[Ljungquist和Bertani,《分子与普通遗传学》192 (1983) 87 - 94]。与原噬菌体不同,int基因在感染性噬菌体中的表达似乎有所不同[Bertani,《美国国家科学院院刊》65 (1970) 331 - 336]。包含int基因和attP、原噬菌体杂合末端attL和attR以及一个细菌附着位点(来自大肠杆菌C菌株的首选位点locI)的一段1200 bp的P2 DNA区域均已测序。一个编码337个氨基酸多肽的开放阅读框对应于int基因。该基因之前没有明显的启动子序列。int基因转录本似乎会延伸至其下游的attP位点之外,这可能为之前观察到的整合与切除差异提供了一种解释。对四个附着位点的比较揭示了一个27 bp的共同“核心”序列:5'-AAAAAATAAGCCCGTGTAAGGGAGATT-3'。发现增加原噬菌体切除的P2 nip1突变位于int基因本身内。具有改变位点偏好的P2 saf变体[Six,《病毒学》29 (1966) 106 - 125]在核心序列内有一个碱基对替换。三个缺失/替换突变体vir22、vir94和del3也有改变的核心序列。