Sanchez G, Mamet-Bratley M D
Département de biochimie, Université de Montréal, Québec, Canada.
Biochem Cell Biol. 1992 Jul;70(7):605-8. doi: 10.1139/o92-092.
The development of bacteriophage T7 was examined in an Escherichia coli double mutant defective for the two major apurinic, apyrimidinic endonucleases (exonuclease III and endonuclease IV, xth nfo). In cells infected with phages containing apurinic sites, the defect in repair enzymes led to a decrease of phage survival and a total absence of bacterial DNA degradation and of phage DNA synthesis. These results directly demonstrate the toxic action of apurinic sites on bacteriophage T7 at the intracellular level and its alleviation by DNA repair. In addition, untreated T7 phage unexpectedly displayed reduced plating efficiency and decreased DNA synthesis in the xth nfo double mutant.
在一种大肠杆菌双突变体中研究了噬菌体T7的发育情况,该双突变体缺乏两种主要的无嘌呤、无嘧啶内切核酸酶(核酸外切酶III和核酸内切酶IV,xth nfo)。在用含有无嘌呤位点的噬菌体感染的细胞中,修复酶的缺陷导致噬菌体存活率降低,细菌DNA降解和噬菌体DNA合成完全缺失。这些结果直接证明了无嘌呤位点在细胞内水平对噬菌体T7的毒性作用以及DNA修复对其的缓解作用。此外,未处理的T7噬菌体在xth nfo双突变体中意外地表现出较低的平板效率和DNA合成减少。