Higgins M L, Daneo-Moore L, Boothby D, Shockman G D
J Bacteriol. 1974 May;118(2):681-92. doi: 10.1128/jb.118.2.681-692.1974.
Selective inhibition of protein synthesis in Streptococcus faecalis (ATCC 9790) was accompanied by a rapid and severe inhibition of cell division and a reduction of enlargement of cellular surface area. Continued synthesis of cell wall polymers resulted in rapid thickening of the wall to an extent not seen in exponential-phase populations. Thus, the normal direction of wall growth was changed from a preferential feeding out of new wall surface to that of thickening existing cell surfaces. However, the overall manner in which the wall thickened, from nascent septa toward polar regions, was the same in both exponential-phase and inhibited populations. In contrast, selective inhibition of deoxyribonucleic acid (DNA) synthesis using mitomycin C was accompanied by an increase in cellular surface area and by division of about 80% of the cells in random populations. Little or no wall thickening was observed until the synthesis of macromolecules other than DNA was impaired and further cell division ceased. Concomitant inhibition of both DNA and protein synthesis inhibited cell division but permitted an increase in average cell volume. In such doubly inhibited cells, walls thickened less than in cells inhibited for protein synthesis only. On the basis of the results obtained, a model for cell surface enlargement and cell division is presented. The model proposes that: (i) each wall enlargement site is influenced by an individual chromosome replication cycle; (ii) during chromosome replication peripheral surface enlargement would be favored over thickening (or septation); (iii) a signal associated with chromosome termination would favor thickening (and septation) at the expense of surface enlargement; and (iv) a factor or signal related to protein synthesis would be required for one or more of the near terminal stages of cell division or cell separation, or both.
粪肠球菌（ATCC 9790）中蛋白质合成的选择性抑制伴随着细胞分裂的快速且严重抑制以及细胞表面积增大的减少。细胞壁聚合物的持续合成导致细胞壁迅速增厚，增厚程度在指数生长期群体中未见。因此，细胞壁生长的正常方向从优先向外添加新的壁表面转变为增厚现有的细胞表面。然而，细胞壁增厚的总体方式，即从新生隔膜向极性区域增厚，在指数生长期群体和受抑制群体中是相同的。相比之下，使用丝裂霉素C选择性抑制脱氧核糖核酸（DNA）合成伴随着细胞表面积的增加以及随机群体中约80%的细胞分裂。在DNA以外的大分子合成受损且进一步的细胞分裂停止之前，几乎没有观察到细胞壁增厚。DNA和蛋白质合成的同时抑制抑制了细胞分裂，但允许平均细胞体积增加。在这种双重抑制的细胞中，细胞壁增厚程度小于仅受蛋白质合成抑制的细胞。基于所获得的结果，提出了一个细胞表面增大和细胞分裂的模型。该模型提出：（i）每个壁增大位点受单个染色体复制周期影响；（ii）在染色体复制期间，外周表面增大将优先于增厚（或隔膜形成）；（iii）与染色体终止相关的信号将优先促进增厚（和隔膜形成），而以表面增大为代价；（iv）细胞分裂或细胞分离的一个或多个近末期阶段，或两者都需要与蛋白质合成相关的因子或信号。
