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噬菌体SPO1感染的枯草芽孢杆菌中的脱氧核糖核酸合成。I. 正常菌株和聚合酶缺陷型菌株中噬菌体脱氧核糖核酸的合成及宿主脱氧核糖核酸的命运

Deoxyribonucleic acid synthesis in bacteriophage SPO1-infected Bacillus subtilis. I. Bacteriophage deoxyribonucleic acid synthesis and fate of host deoxyribonucleic acid in normal and polymerase-deficient strains.

作者信息

Yehle C O, Ganesan A T

出版信息

J Virol. 1972 Feb;9(2):263-72. doi: 10.1128/JVI.9.2.263-272.1972.

Abstract

The effect of bacteriophage SPO1 infection of Bacillus subtilis and a deoxyribonucleic acid (DNA) polymerase-deficient (pol(-)) mutant of this microorganism on the synthesis of DNA has been examined. Soon after infection, the incorporation of deoxyribonucleoside triphosphates into acid-insoluble material by cell lysates was greatly reduced. This inhibition of host DNA synthesis was not a result of host chromosome degradation nor did it appear to be due to the induction of thymidine triphosphate nucleotidohydrolase. Examination of the host chromosome for genetic linkage throughout the lytic cycle indicated that no extensive degradation occurred. After the inhibition of host DNA synthesis, a new polymerase activity arose which directed the synthesis of phage DNA. This new activity required deoxyribonucleoside triphosphates as substrates, Mg(2+) ions, and a sulfhydryl reducing agent, and it was stimulated in the presence of adenosine triphosphate. The phage DNA polymerase, like that of its host, was associated with a fast-sedimenting cell membrane complex. The pol(-) mutation had no effect on the synthesis of phage DNA or production of mature phage particles.

摘要

已研究了噬菌体SPO1感染枯草芽孢杆菌及其该微生物的脱氧核糖核酸(DNA)聚合酶缺陷型(pol(-))突变体对DNA合成的影响。感染后不久,细胞裂解物将脱氧核苷三磷酸掺入酸不溶性物质的过程大大减少。宿主DNA合成的这种抑制不是宿主染色体降解的结果,也似乎不是由于三磷酸胸苷核苷酸水解酶的诱导。在整个裂解周期中对宿主染色体进行遗传连锁检查表明没有发生广泛降解。宿主DNA合成受到抑制后,出现了一种新的聚合酶活性,该活性指导噬菌体DNA的合成。这种新活性需要脱氧核苷三磷酸作为底物、镁离子和巯基还原剂,并且在三磷酸腺苷存在下会受到刺激。噬菌体DNA聚合酶与其宿主的聚合酶一样,与快速沉降的细胞膜复合物相关。pol(-)突变对噬菌体DNA的合成或成熟噬菌体颗粒的产生没有影响。

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