Henning U, Dennert G, Rehn K, Deppe G
J Bacteriol. 1969 May;98(2):784-96. doi: 10.1128/jb.98.2.784-796.1969.
The effects of oleate starvation on an oleate auxotroph of Escherichia coli K-12 were investigated. Following removal of oleate from the mutant growing in a minimal glycerol-peptone medium, the cells stopped making deoxyribonucleic acid, ribonucleic acid, protein, and phospholipids; they began to die exponentially and finally lysed. During oleate starvation in minimal medium minus peptone, inhibition of macromolecular syntheses and death occurred; however, lysis did not follow. When growth ceased, no further dying was observed. It is shown that none of the early effects (inhibition of macromolecular syntheses and death) can be due to leakiness of the cells, induction of a prophage or a colicin, or lack of energy sources. The cause of inhibition of macromolecular syntheses remained unknown. Since the rate of death was the same as the generation time under different conditions, it appears that death is due to the defective synthesis of some cellular structure (quite possibly, cytoplasmic membrane) during phospholipid deficiency. Lysis was found to require protein synthesis; electron microscopy revealed a peculiar type of "lysis from within"; i.e., the shape of the cells did not change but fragmentation of the inner layer of the cell envelope occurred. The murein was found to be unaltered. Most likely, lysis was a consequence of the cell's attempt to synthesize cytoplasmic membrane with altered phospholipid composition or during phospholipid deficiency. Several membrane functions (respiration, adenosine triphosphate formation, permeability) existing before oleate removal were not lost during starvation. Therefore, general damage to the membrane did not occur, and it could be that most, if not all, described effects were due to defective de novo membrane synthesis.
研究了油酸饥饿对大肠杆菌K - 12油酸营养缺陷型的影响。在从生长于基本甘油 - 蛋白胨培养基中的突变体中去除油酸后,细胞停止合成脱氧核糖核酸、核糖核酸、蛋白质和磷脂;它们开始呈指数级死亡,最终裂解。在不含蛋白胨的基本培养基中进行油酸饥饿时,大分子合成受到抑制且细胞死亡,但随后并未发生裂解。当生长停止时,未观察到进一步的死亡现象。结果表明,早期效应(大分子合成抑制和细胞死亡)均不是由于细胞渗漏、原噬菌体或大肠杆菌素的诱导,也不是由于缺乏能源所致。大分子合成受抑制的原因尚不清楚。由于在不同条件下细胞死亡速率与代时相同,似乎细胞死亡是由于磷脂缺乏期间某些细胞结构(很可能是细胞质膜)合成缺陷所致。发现裂解需要蛋白质合成;电子显微镜显示出一种特殊类型的“自内裂解”;即细胞形状未改变,但细胞包膜内层发生了碎片化。发现胞壁质未发生改变。裂解很可能是细胞试图在磷脂组成改变或磷脂缺乏期间合成细胞质膜的结果。在去除油酸之前存在的几种膜功能(呼吸作用、三磷酸腺苷形成、通透性)在饥饿期间并未丧失。因此,膜并未受到普遍损伤,而且很可能所描述的大多数(如果不是全部)效应是由于从头合成膜存在缺陷所致。