Stafford M E, Reddy G P, Mathews C K
J Virol. 1977 Jul;23(1):53-60. doi: 10.1128/JVI.23.1.53-60.1977.
This paper describes several technical improvements in the sucrose-plasmolyzed cell system used in earlier experiments on DNA synthesis in situ with Escherichia coli infected by DNA-defective mutants of bacteriophage T4 (W. L. Collinsworth and C. K. Mathews, J. Virol. 13:908-915, 1974). Using this system, which is based primarily on that of M. G. Wovcha et al. (Proc. Natl. Acad. Sci. U.S.A. 70:2196-2200, 1973), we reinvestigated the properties of mutants bearing lesions in genes 1, 41, and 62, and we resolved some disagreements with data reported from that laboratory. We also asked whether the DNA-delay phenotype of T4 mutants is related to possible early leakage of DNA precursors from infected cells. Such cells display defective DNA synthesis in situ, even when ample DNA precursors are made available. Thus, the lesions associated with these mutations seem to manifest themselves at the level of macromolecular metabolism. Similarly, we examined an E. coli mutant defective in its ability to support T4 production, apparently because of a lesion affecting DNA synthesis (L. Simon et al., Nature [London] 252:451-455). In the plasmolyzed cell system, reduced nucleotide incorporation is seen, indicating also that the genetic defect does not involve DNA precursor synthesis. The plasmolyzed cell system incorporates deoxynucleotide 5'-monophosphates into DNA severalfold more rapidly than the corresponding 5'-triphosphates. This is consistent with the idea that DNA precursor-synthesizing enzymes are functionally organized to shuttle substrates to their sites of utilization.
本文描述了蔗糖质壁分离细胞系统的几项技术改进,该系统用于早期关于用噬菌体T4的DNA缺陷突变体感染的大肠杆菌进行原位DNA合成的实验(W. L. 柯林斯沃思和C. K. 马修斯,《病毒学杂志》13:908 - 915,1974)。使用这个主要基于M. G. 沃查等人(《美国国家科学院院刊》70:2196 - 2200,1973)的系统,我们重新研究了在基因1、41和62中存在损伤的突变体的特性,并解决了与该实验室报道的数据存在的一些分歧。我们还询问了T4突变体的DNA延迟表型是否与感染细胞中DNA前体可能的早期泄漏有关。即使提供充足的DNA前体,这些细胞在原位仍显示出有缺陷的DNA合成。因此,与这些突变相关的损伤似乎在大分子代谢水平上表现出来。同样,我们研究了一种大肠杆菌突变体,它支持T4产生的能力存在缺陷,显然是由于影响DNA合成的损伤(L. 西蒙等人,《自然》[伦敦]252:451 - 455)。在质壁分离细胞系统中,观察到核苷酸掺入减少,这也表明遗传缺陷不涉及DNA前体合成。质壁分离细胞系统将脱氧核苷酸5'-单磷酸掺入DNA的速度比相应的5'-三磷酸快几倍。这与DNA前体合成酶在功能上被组织起来将底物穿梭到其利用位点的观点一致。