INTERGENIC REGION AND THE ORIGINS FOR FILAMENTOUS PHAGE DNA-REPLICATION
INTERGENIC REGION AND THE ORIGINS FOR FILAMENTOUS PHAGE DNA-REPLICATION
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DOI：
10.1101/sqb.1979.043.01.046
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发表时间：
1979-01-01
期刊：
影响因子：
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通讯作者：
SCHALLER, H
中科院分区：
文献类型：
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作者：
SCHALLER, H
具有单链基因组的噬菌体，如~ bX174和fd，在被感染的细胞中开始它们的生命周期，将它们的病毒环状DNA转化为共价封闭的、双链的亲本复制形式（RF） DNA（阶段1，单链到双链[SS~ DS] DNA复制）。下一阶段的生长需要一种噬菌体编码的蛋白，该蛋白将在起始点切割RF DNA，并将其作为宿主蛋白进一步复制的底物（第二阶段，DS~ DS DNA复制）。在最后阶段，噬菌体蛋白使病毒链复合，限制互补链的形成，并允许含有病毒DNA环的子代病毒组装（第三阶段，DS-~ SS DNA复制）。丝状噬菌体不能溶解被感染的宿主细胞。它们的基因组作为“多拷贝质粒”在许多代细菌中繁殖，同时从受感染的宿主释放噬菌体后代。由于这种寄生生命周期，DNA复制的第二和第三阶段以一种耦合和平衡的方式同时发生，因此在受感染细胞中保持了高拷贝数的DS和SS DNA分子。这两种DNA合成模式的比例由病毒基因v蛋白的水平控制，这是一种DNA结合蛋白（DBP），似乎会干扰互补链的合成（Mazur和Model 1973）。病毒链合成的起始反过来由基因ii蛋白控制，基因ii蛋白是一种病毒起始因子，其作用是链特异性的缺口活性（Fidanifin和Ray 1972； Geider和Meyer，本卷）。在噬菌体增殖的所有阶段，DNA复制都是在一个不同的位点开始的，这可以从体内脉冲标记后新合成的DNA分布在完整的噬菌体DNA分子中得到证明（Horiuchi and Zinder 1976; Suggs and Ray 1977）。在使用的方法范围内，发现病毒链和互补链的起始位点是相同的，其图谱位置与体外确定的病毒DNA开始SS~ DS转化的位置一致（Tabak et al. 1974; Schaller et al. 1976）。由于体外复制系统的改进（Geider and Meyer，本卷）和噬菌体基因组核苷酸序列的测定（Schaller et al. 1978），关于起源的结构和功能的新信息最近变得可用。目的
Phages that have a single-stranded genome, such as~ bX174 and fd, begin their life cycles in infected cells with the conversion of their viral circular DNA into the covalently closed, duplex, parental replicative form (RF) DNA (stage I, single-stranded to double-stranded [SS~ DS] DNA replication). The next stage of growth requires a phage-coded protein that will nick the RF DNA at the origin and prepare it as a substrate for further replication by host proteins (stage II, DS~ DS DNA replication). In the last stage, phage proteins complex the viral strand, restrict the formation of complementary strands, and allow the assembly of progeny virus containing the viral DNA circle (stage III, DS-~ SS DNA replication). Filamentous bacteriophages do not lyse the infected host cell. Their genome is propagated as a" multicopy plasmid" through many bacterial generations, with a concomitant release of phage progeny from the infected host. As a consequence of this parasital life cycle, stages II and III of DNA replication occur simultaneously in a coupled and well-balanced manner, so that a high copy number of DS and SS DNA molecules is maintained in the infected cell. The ratio of the two modes of DNA synthesis is controlled by the level of viral gene-V protein, a DNA-binding protein (DBP) which appears to interfere with complementary-strand synthesis (Mazur and Model 1973). Initiation of viral-strand synthesis is in turn controlled by gene-II protein, a viral initiation factor which acts as a strand-specific nicking activity (Fidanifin and Ray 1972; Geider and Meyer, this volume). During all stages of phage multiplication, DNA replication is initiated at a distinct site, as indicated by the distribution of newly synthesized DNA in completed phage DNA molecules after pulse labeling in vivo (Horiuchi and Zinder 1976; Suggs and Ray 1977). Within the limits of the method used, this initiation site was found to be the same for both the viral strand and the complementary strand, and its map position coincides with the one determined in vitro for the start of SS~ DS conversion of viral DNA (Tabak et al. 1974; Schaller et al. 1976). New information on the structure and function of the origin has recently become available as a result of the improvement of in vitro replication systems (Geider and Meyer, this volume) and the determination of the nucleotide sequence of the phage genome (Schaller et al. 1978). The purpose