质粒R1的失控复制并非由基因cop的复制抑制活性丧失所致。
Runaway replication of plasmid R1 is not caused by loss of replication inhibitor activity of gene cop.
作者信息
Molin S, Diaz R, Uhlin B E, Nordström K
出版信息
J Bacteriol. 1980 Aug;143(2):1046-8. doi: 10.1128/jb.143.2.1046-1048.1980.
Abstract
The replication control functions of a mutant of plasmid R1 that replicates without control at temperatures above 35 degrees C have been analyzed. Although the mutations have not been mapped precisely, the data indicate that the gene (cop) previously identified on the wild-type plasmid (S. Molin and K. Nordström, J. Bacteriol. 141:111-120, 1980) as being responsible for expressing a trans-acting replication inhibitor, as well as for incompatibility of plasmid R1, is not affected in this mutant. Thus, the conditional lack of replication control observed in this plasmid mutant presumably is not caused by the loss of inhibitor activity of the cop gene.
摘要
对质粒R1的一个突变体的复制控制功能进行了分析，该突变体在温度高于35摄氏度时不受控制地进行复制。尽管这些突变尚未精确定位，但数据表明，先前在野生型质粒上鉴定出的负责表达反式作用复制抑制剂以及质粒R1不相容性的基因（cop）在该突变体中未受影响。因此，在该质粒突变体中观察到的复制控制的条件性缺失大概不是由cop基因抑制剂活性的丧失引起的。
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