Site-specific Recombination of Bacteriophage λ: The Role of Host Gene Products
Site-specific Recombination of Bacteriophage λ: The Role of Host Gene Products
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噬菌体 λ 的位点特异性重组：宿主基因产物的作用
DOI：
10.1101/sqb.1979.043.01.125
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发表时间：
1979
期刊：
影响因子：
--
通讯作者：
D. Friedman
中科院分区：
文献类型：
--
作者：
H. Miller;A. Kikuchi;H. Nash;R. Weisberg;D. Friedman
噬菌体A的DNA整合到大肠杆菌的染色体上是通过两个独特的基因位点的重组发生的：噬菌体基因组上的attP和细菌染色体上的attB。因此，该反应是位点特异性重组的一个例子。在这些附着位点重组所需的唯一噬菌体编码蛋白是噬菌体Int基因的产物。A的整合产生了一个前体，它的两侧是两个新的att位点，attL和attR。先前已经证明，除了噬菌体编码的蛋白质外，一个或多个宿主基因的产物对于位点特异性重组也是必需的（Miller and Friedman 1977a; Nash et al. 1977; Williams et al. 1977）。在本文中，我们简要地介绍了实验结果，这些结果表征了无法进行A位点特异性重组的突变大肠杆菌菌株。我们的研究描述了这些菌株整合缺陷的生化性质，并确定了负责的遗传位点。对这些新发现的基因座的兴趣有望超越对A位点特异性重组的研究，因为突变体表现出各种其他表型，其中一些似乎不是重组缺陷的结果。
Integration of the DNA of bacteriophage A into the chromosome of Escherichia coli occurs by recombination at two unique genetic loci: attP on the phage genome and attB on the bacterial chromosome. This reaction is therefore an example of site-specific recombination. The only phage-encoded protein required for recombination at these art (attachment) sites is Int, the product of the phage int gene. Integration of A generates a prophage that is flanked by two new att sites, attL and attR. Excision, recombination between attL and attR, requires Xis, the product of the phage xis gene, as well as Int (for review, see Weisberg et al. 1977). It has previously been demonstrated that in addition to phage-encoded proteins, the products of one or more host genes are necessary for A site-specific recombination (Miller and Friedman 1977a; Nash et al. 1977; Williams et al. 1977). In this paper, we briefly present the results of experiments that characterize mutant E. coli strains that are unable to carry out A site-specific recombination. Our studies describe the biochemical nature of the integration defect in these strains and define the genetic loci that are responsible. The interest in these newly identified genetic loci promises to extend beyond the study of A site-specific recombination, since the mutants exhibit various other phenotypes, some of which do not appear to be a consequence of a defect in recombination.