PLASMID ADDICTION GENES OF BACTERIOPHAGE-P1 - DOC, WHICH CAUSES CELL-DEATH ON CURING OF PROPHAGE, AND PHD, WHICH PREVENTS HOST DEATH WHEN PROPHAGE IS RETAINED
PLASMID ADDICTION GENES OF BACTERIOPHAGE-P1 - DOC, WHICH CAUSES CELL-DEATH ON CURING OF PROPHAGE, AND PHD, WHICH PREVENTS HOST DEATH WHEN PROPHAGE IS RETAINED
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DOI：
10.1006/jmbi.1993.1521
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发表时间：
1993-10-05
影响因子：
5.6
通讯作者：
YARMOLINSKY, MB
中科院分区：
文献类型：
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作者：
LEHNHERR, H;MAGUIN, E;YARMOLINSKY, MB
大肠杆菌P1溶原菌将原噬菌体作为稳定的低拷贝质粒。产生去除原噬菌体的活细胞的频率约为每代每个细胞10- 5个。在这里，我们表明，这种显着的稳定性的一个重要部分可以归因于质粒编码的机制，导致死亡的细胞已经失去了P1。换句话说，溶原性细胞似乎对原噬菌体的存在上瘾。质粒撤回反应依赖于一个名为deddoc（deathoncuring）的基因，编码一个126个氨基酸的蛋白质。Doc的表达不是SOS诱导的，Doc的杀伤是recA非依赖性的。在保留了P1的细胞中，一种名为“预防死亡”（preventhostdeath）的基因产物阻止了这种杀伤，该基因编码一种73个氨基酸的蛋白质。从P1 DNA的0.7kb片段中克隆并表达了该基因。这两个基因构成了一个操纵子，Doc的合成似乎与Phd的合成在功能上偶联。P1成瘾基因的同源物在别处也有发现，但与先前描述的其他质粒的基因无关，这些基因也通过分离后杀伤引起质粒稳定性的明显增加。
P1 lysogens ofEscherichia colicarry the prophage as a stable low copy number plasmid. The frequency with which viable cells cured of prophage are produced is about 10-5per cell per generation. Here we show that a significant part of this remarkable stability can be attributed to a plasmid encoded mechanism that causes death of cells that have lost P1. In other words, the lysogenic cells appear to be addicted to the presence of the prophage. The plasmid withdrawal response depends on a gene nameddoc(deathoncuring), encoding a 126 amino acid protein. Expression ofdocis not SOS-inducing and killing by Doc isrecA-independent. In cells that, retain P1 the killing is prevented by the product of a gene namedphd(preventhostdeath), encoding a 73 amino acid protein. The genesphdanddochave been cloned and expressed from a 0·7 kb segment of P1 DNA. The two genes constitute an operon and the synthesis of Doc appears to be translationally coupled to that of Phd. Homologs of the P1 addiction genes are found elsewhere, butphdanddocare unrelated to previously described genes of other plasmids that also cause an apparent increase in plasmid stability by post-segregational killing.