Keweloh H W, Bakker E P
J Bacteriol. 1984 Oct;160(1):354-9. doi: 10.1128/jb.160.1.354-359.1984.
The addition of T1 to cells growing at 37 degrees C in a minimal medium at 0.4 mM Mg2+ rapidly induced an irreversible loss of K+ and Mg2+ and uptake of Na+ by the cells. Both the ATP pool of the cells and the transmembrane proton motive force were reduced. These cells did not lyse from within, since viral DNA replication and the maturation of the 36,000-molecular-weight phage head protein were inhibited. By contrast, cells lysed when infected at 5.4 mM Mg2+. In these cells, T1 initially induced K+ efflux and Na+ influx and lowered the cytoplasmic ATP concentration. After a few minutes, the cation gradients and ATP pool were restored to levels close to that of control cells. At 5.4 mM Mg2+, the shutoff of host protein synthesis was delayed and coincided with the restoration of the ATP pool. In an ATP synthase-negative mutant, infection with T1 did not affect the cytoplasmic ATP concentration but inhibited host protein synthesis with the same rate as it did in wild-type cells.
在含有0.4 mM Mg2+的基本培养基中，于37摄氏度生长的细胞加入T1后，会迅速导致细胞内K+和Mg2+的不可逆丢失以及Na+的摄取。细胞的ATP池和跨膜质子动力均降低。这些细胞不会从内部裂解，因为病毒DNA复制和36,000分子量噬菌体头部蛋白的成熟受到抑制。相比之下，在5.4 mM Mg2+条件下感染时细胞会裂解。在这些细胞中，T1最初诱导K+外流和Na+内流，并降低细胞质ATP浓度。几分钟后，阳离子梯度和ATP池恢复到接近对照细胞的水平。在5.4 mM Mg2+时，宿主蛋白合成的关闭延迟，且与ATP池的恢复同时发生。在一个ATP合酶阴性突变体中，用T1感染不会影响细胞质ATP浓度，但以与野生型细胞相同的速率抑制宿主蛋白合成。
