Willis D B, Ennis H L
J Virol. 1969 Jan;3(1):1-7. doi: 10.1128/JVI.3.1.1-7.1969.
A mutant of Bacillus subtilis 168 (strain 168 KW), defective in its ability to concentrate K(+) from low levels in the growth medium, was used to study the role of K(+) in the development of phage 2C. Both the final burst size and the duration of the rise period depended on the K(+) concentration in the medium. During normal infection (in the presence of K(+)), host deoxyribonucleic acid (DNA) synthesis stopped. The synthesis of host messenger ribonucleic acid (RNA) continued throughout infection, albeit at a steadily decreasing rate. The synthesis of ribosomal RNA and its subsequent incorporation into mature ribosomes also proceeded. In contrast to these findings, host DNA and messenger RNA synthesis were not inhibited in cells infected in the absence of K(+). Only "early" phage messenger RNA was synthesized under these conditions of infection. Phage DNA synthesis was dependent on K(+) irrespective of the requirement for this cation in protein synthesis.
枯草芽孢杆菌168(168 KW菌株)的一个突变体,其从生长培养基中低水平浓缩钾离子(K⁺)的能力存在缺陷,被用于研究K⁺在噬菌体2C发育中的作用。最终的裂解量和上升期的持续时间都取决于培养基中的K⁺浓度。在正常感染期间(存在K⁺时),宿主脱氧核糖核酸(DNA)合成停止。宿主信使核糖核酸(RNA)的合成在整个感染过程中持续进行,尽管速率在稳步下降。核糖体RNA的合成及其随后掺入成熟核糖体的过程也在进行。与这些发现相反,在没有K⁺的情况下感染的细胞中,宿主DNA和信使RNA的合成并未受到抑制。在这些感染条件下,只合成了“早期”噬菌体信使RNA。噬菌体DNA的合成依赖于K⁺,而与蛋白质合成中对这种阳离子的需求无关。