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大肠杆菌中累积的L-α-甘油磷酸导致生长停滞。

Growth stasis by accumulated L-alpha-glycerophosphate in Escherichia coli.

作者信息

Cozzarelli N R, Koch J P, Hayashi S, Lin E C

出版信息

J Bacteriol. 1965 Nov;90(5):1325-9. doi: 10.1128/jb.90.5.1325-1329.1965.

Abstract

Cozzarelli, N. R. (Harvard Medical School, Boston, Mass.), J. P. Koch, S. Hayashi, and E. C. C. Lin. Growth stasis by accumulated l-alpha-glycerophosphate in Escherichia coli. J. Bacteriol. 90:1325-1329.1965.-Cells of Escherichia coli K-12 can grow on either glycerol or l-alpha-glycerophosphate as the sole source of carbon and energy. The first step in the dissimilation of glycerol requires a kinase, and the initial process of utilization of l-alpha-glycerophosphate involves an active transport system. In either case, intracellular l-alpha-glycerophosphate is an intermediate whose further metabolism depends upon a dehydrogenase. When this enzyme is lost by mutation, the cells not only fail to grow on glycerol or l-alpha-glycerophosphate, but are subject to growth inhibition in the presence of either compound. Resistance to inhibition by glycerol can be achieved by the loss of glycerol kinase. Such cells are still susceptible to growth inhibition by l-alpha-glycerophosphate. Similarly, in dehydrogenase-deficient cells, immunity to exogenous l-alpha-glycerophosphate can be achieved by genetic blocking of the active transport system. Such cells are still sensitive to free glycerol in the growth medium. Reversal of inhibition by glycerol or l-alpha-glycerophosphate in cells lacking the dehydrogenase can also be brought about by the addition of glucose. Glucose achieves this effect without recourse to catabolite repression. Our results suggest that growth stasis associated with the over-accumulation of l-alpha-glycerophosphate is due to interference with other cellular processes by competition with physiological substrates rather than to depletion of cellular stores of adenosine triphosphate or inorganic phosphate.

摘要

科扎雷利,N. R.(哈佛医学院,马萨诸塞州波士顿),J. P. 科赫,S. 林,E. C. C. 林。大肠杆菌中累积的L-α-甘油磷酸导致生长停滞。《细菌学杂志》90:1325 - 1329.1965。 - 大肠杆菌K - 12细胞能够以甘油或L-α-甘油磷酸作为唯一碳源和能源生长。甘油异化的第一步需要一种激酶,而L-α-甘油磷酸的初始利用过程涉及一个主动运输系统。在任何一种情况下,细胞内的L-α-甘油磷酸都是一种中间产物,其进一步代谢取决于一种脱氢酶。当这种酶因突变而缺失时,细胞不仅不能在甘油或L-α-甘油磷酸上生长,而且在这两种化合物存在的情况下会受到生长抑制。通过缺失甘油激酶可以实现对甘油抑制的抗性。这样的细胞仍然易受L-α-甘油磷酸的生长抑制。同样,在缺乏脱氢酶的细胞中,通过对主动运输系统进行基因阻断可以实现对外源L-α-甘油磷酸的免疫。这样的细胞仍然对生长培养基中的游离甘油敏感。在缺乏脱氢酶的细胞中,添加葡萄糖也可以逆转甘油或L-α-甘油磷酸的抑制作用。葡萄糖实现这种效果无需依赖分解代谢物阻遏。我们的结果表明,与L-α-甘油磷酸过度积累相关的生长停滞是由于与生理底物竞争而干扰了其他细胞过程,而不是由于细胞内三磷酸腺苷或无机磷酸盐储备的耗尽。

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