Sayare M, Daneo-Moore L, Shockman G D
J Bacteriol. 1972 Oct;112(1):337-44. doi: 10.1128/jb.112.1.337-344.1972.
The addition of several different antibiotics to growing cultures of Streptococcus faecalis, ATCC 9790, was found to inhibit autolysis of cells in sodium phosphate buffer. When added to exponential-phase cultures, mitomycin C (0.4 mug/ml) or phenethyl alcohol (3 mg/ml) inhibited deoxyribonucleic acid synthesis, but did not appreciably affect the rate of cellular autolysis. Addition of chloramphenicol (10 mug/ml), tetracycline (0.5 mug/ml), puromycin (25 mug/ml), or 5-azacytidine (5 mug/ml) to exponential-phase cultures inhibited protein synthesis and profoundly decreased the rate of cellular autolysis. Actinomycin D (0.075 mug/ml) and rifampin (0.01 mug/ml), both inhibitors of ribonucleic acid (RNA) synthesis, also reduced the rate of cellular autolysis. However, the inhibitory effect of actinomycin D and rifampin on cellular autolysis was more closely correlated with their concomitant secondary inhibition of protein synthesis than with the more severe inhibition of RNA synthesis. The dose-dependent inhibition of protein synthesis by 5-azacytidine was quickly diluted out of a growing culture. Reversal of inhibition was accompanied by a disproportionately rapid increase in the ability of cells to autolyze. Thus, inhibition of the ability of cells to autolyze can be most closely related to inhibition of protein synthesis. Furthermore, the rapidity of the response of cellular autolysis to inhibitors of protein synthesis suggests that regulation is exerted at the level of autolytic enzyme activity and not enzyme synthesis.
研究发现,向粪肠球菌(ATCC 9790)的生长培养物中添加几种不同的抗生素,可抑制其在磷酸钠缓冲液中的细胞自溶。当添加到指数生长期培养物中时,丝裂霉素C(0.4微克/毫升)或苯乙醇(3毫克/毫升)抑制脱氧核糖核酸合成,但对细胞自溶速率没有明显影响。向指数生长期培养物中添加氯霉素(10微克/毫升)、四环素(0.5微克/毫升)、嘌呤霉素(25微克/毫升)或5-氮杂胞苷(5微克/毫升)可抑制蛋白质合成,并显著降低细胞自溶速率。放线菌素D(0.075微克/毫升)和利福平(0.01微克/毫升)这两种核糖核酸(RNA)合成抑制剂,也降低了细胞自溶速率。然而,放线菌素D和利福平对细胞自溶的抑制作用与其伴随的对蛋白质合成的二次抑制更为密切相关,而不是与对RNA合成的更严重抑制相关。5-氮杂胞苷对蛋白质合成的剂量依赖性抑制在生长培养物中很快被稀释掉。抑制作用的逆转伴随着细胞自溶能力不成比例的快速增加。因此,细胞自溶能力的抑制与蛋白质合成的抑制关系最为密切。此外,细胞自溶对蛋白质合成抑制剂的快速反应表明,调节作用是在自溶酶活性水平而非酶合成水平上发挥的。