Higgins M L, McDowell T D, Sleytr U B, Mychajlonka M, Shockman G D
J Bacteriol. 1980 Dec;144(3):1168-73. doi: 10.1128/jb.144.3.1168-1173.1980.
Strains of Streptococcus mutans are very susceptible to growth inhibition by benzylpenicillin, but are tolerant to lysis when exposed to even high concentrations of this drug. These properties enabled this study of S. mutans GS-5 surface growth and peptidoglycan, ribonucleic acid, protein, and deoxyribonucleic acid syntheses in the absence of osmotic stabilization. Inhibition of syntheses of peptidoglycan, ribonucleic acid, and protein was dose dependent. Synthesis of peptidoglycan was most susceptible. Substantial but less severe inhibitions of ribonucleic acid and protein syntheses rapidly followed decreased peptidoglycan synthesis, whereas inhibition of deoxyribonucleic acid synthesis was delayed and minimal. Computer-assisted reconstructions of surface growth zones and poles observed in electron micrographs of replicas were performed and indicated that at low concentrations of benzylpenicillin (0.03 micrograms/ml), growth sites reached abnormally large sizes and surface/volume ratios. The observed shifts in surface/volume ratio were attributed to an inhibition of the normal constrictive division mechanism. The poles of these cells also increased in size over those of the controls, but the relatively smaller change in surface/volume ratio confirmed the visual impression that the shape of the poles was much less altered than the shape of the growth sites. As the concentration of benzylpenicillin used was raised from 0.03 to 2 micrograms/ml, the ability of growth sites and poles to enlarge was restricted in a manner that most closely agreed with the extent of inhibition of peptidoglycan (rather than deoxyribonucleic acid, ribonucleic acid, or protein) synthesis. This correlation suggested that increases in cell size may be regulated by the supply of peptidoglycan precursors.
变形链球菌菌株对苄青霉素的生长抑制非常敏感,但即使暴露于高浓度的这种药物下也能耐受裂解。这些特性使得在没有渗透稳定作用的情况下,能够对变形链球菌GS-5的表面生长以及肽聚糖、核糖核酸、蛋白质和脱氧核糖核酸的合成进行这项研究。肽聚糖、核糖核酸和蛋白质合成的抑制呈剂量依赖性。肽聚糖合成最敏感。随着肽聚糖合成减少,核糖核酸和蛋白质合成迅速受到显著但不太严重的抑制,而脱氧核糖核酸合成的抑制则延迟且程度最小。对复制品电子显微照片中观察到的表面生长区和极进行了计算机辅助重建,结果表明,在低浓度苄青霉素(0.03微克/毫升)下,生长位点达到异常大的尺寸和表面/体积比。观察到的表面/体积比的变化归因于正常收缩分裂机制的抑制。这些细胞的极也比对照细胞的极增大了,但表面/体积比相对较小的变化证实了视觉印象,即极的形状变化远小于生长位点的形状变化。随着所用苄青霉素浓度从0.03微克/毫升提高到2微克/毫升,生长位点和极增大的能力受到限制,其方式与肽聚糖(而非脱氧核糖核酸、核糖核酸或蛋白质)合成的抑制程度最为一致。这种相关性表明,细胞大小的增加可能受肽聚糖前体供应的调节。