Satta G, Botta G, Canepari P, Fontana R
J Bacteriol. 1981 Oct;148(1):10-9. doi: 10.1128/jb.148.1.10-19.1981.
The effects of mecillinam on the growth of rods of the pH-conditional morphology mutant MirM7 was studied. It has been found that mecillinam causes, coincident with transition to coccal shape, a balanced rise in the rate of viable count increase and the rate of macromolecular synthesis which lasts either until the cells enter a stationary growth phase or indefinitely, in the case of continuously diluted cultures. When the antibiotic is removed from cells which have already become coccoid, cells continue to grow at a faster rate until they resume the rod shape. No change in the per-cell rate of protein synthesis has been seen in untreated or mecillinam-treated cells before or after the change in growth rate. Studies with synchronously growing cells have shown that the antibiotic causes a shortening in the I period (initiation of deoxyribonucleic acid replication). Evaluation of the residual divisions in nalidixic acid-treated, exponential-phase cells has shown that mecillinam also shortens the D period (cell division). It is proposed that, in strain MirM7, inhibition of lateral wall elongation by the antibiotic allows the initiation of a new septum, though inhibition is still in progress. The initiation of a new septum is, in turn, responsible for both the early inibition of deoxyribonucleic acid replication and accelerated division. In the parental strain, MirA12, as well as in other sensitive gram-negative rods which divide, become cocci, and stop dividing after addition of the antibiotic, inhibition of lateral wall formation activates a feedback mechanism which prevents insertion of new septa (Satta et al., J. Bacteriol. 142:43-51, 1980). Consequently, no early initiation of deoxyribonucleic acid replication is observed, and the last division allowed by the antibiotic occurs in due time. This negative control is missing in MirM7.
研究了美西林对pH条件形态突变体MirM7杆菌生长的影响。已发现,美西林在导致细胞转变为球菌形状的同时,活菌数增加速率和大分子合成速率平衡上升,这种上升持续到细胞进入稳定生长期,或者在连续稀释培养的情况下无限期持续。当从已经变成球菌的细胞中去除抗生素时,细胞继续以更快的速率生长,直到恢复杆状形态。在生长速率改变之前或之后,未处理或经美西林处理的细胞中,每细胞蛋白质合成速率均未发生变化。对同步生长细胞的研究表明,抗生素会使I期(脱氧核糖核酸复制起始)缩短。对萘啶酸处理的指数生长期细胞中剩余分裂的评估表明,美西林也会缩短D期(细胞分裂期)。有人提出,在MirM7菌株中,抗生素对侧壁伸长的抑制作用允许新隔膜的起始,尽管抑制作用仍在进行中。新隔膜的起始反过来又导致脱氧核糖核酸复制的早期抑制和加速分裂。在亲本菌株MirA12以及其他敏感的革兰氏阴性杆菌中,添加抗生素后,这些杆菌分裂、变成球菌并停止分裂,侧壁形成的抑制激活了一种反馈机制,阻止新隔膜的插入(Satta等人,《细菌学杂志》142:43 - 51,1980年)。因此,未观察到脱氧核糖核酸复制的早期起始,抗生素允许的最后一次分裂在适当的时候发生。而MirM7中缺少这种负调控。