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大肠杆菌中磷脂生物合成停止期间脂肪酸合成的调控。

Regulation of fatty acid synthesis during the cessation of phospholipid biosynthesis in Escherichia coli.

作者信息

Nunn W D, Kelly D L, Stumfall M Y

出版信息

J Bacteriol. 1977 Nov;132(2):526-31. doi: 10.1128/jb.132.2.526-531.1977.

Abstract

In 1975, Cronan et al. (J. Biol. Chem. 250:5835-5840) reported that free fatty acids accumulated during glycerol starvation of an Escherichia coli glycerol auxotroph. On the basis of labeling experiments showing significant incorporation of [14C]acetate into the fatty acid fraction of glycerol-starved cells, these authors concluded that fatty acid synthesis proceeded normally in the absence of phospholipid synthesis. Since these findings might have been due to an increase in the intracellular specific activity of the [1-14C]acetyl coenzyme A pool of the glycerol-starved cells, we reexamined the effect of glycerol starvation on fatty acid synthesis. We found that (i) the incorporation of 3H2O and/or [2,3-14C]succinate into the fatty acid fraction of glycerol auxotrophs is severely reduced during starvation, (ii) the incorporation of [1-14C]acetate into the lipid fraction of an acetate-requiring glycerol auxotroph is inhibited by 95% during glycerol starvation, and (iii) the accumulation of fatty acids, as measured by microtitration, in glycerol-starved cells is less than 10% that of glycerol-supplemented cells. These results indicate that fatty acid synthesis is inhibited in the absence of phospholipid synthesis of E. coli.

摘要

1975年,克罗南等人(《生物化学杂志》250:5835 - 5840)报道,在大肠杆菌甘油营养缺陷型菌株甘油饥饿期间,游离脂肪酸会积累。基于标记实验表明[14C]乙酸盐大量掺入甘油饥饿细胞的脂肪酸部分,这些作者得出结论,在没有磷脂合成的情况下,脂肪酸合成仍正常进行。由于这些发现可能是由于甘油饥饿细胞中[1 - 14C]乙酰辅酶A池的细胞内比活性增加所致,我们重新研究了甘油饥饿对脂肪酸合成的影响。我们发现:(i)在饥饿期间,甘油营养缺陷型菌株中3H2O和/或[2,3 - 14C]琥珀酸盐掺入脂肪酸部分的量严重减少;(ii)在甘油饥饿期间,需要乙酸盐的甘油营养缺陷型菌株中[1 - 14C]乙酸盐掺入脂质部分的量被抑制了95%;(iii)通过微量滴定法测量,甘油饥饿细胞中脂肪酸的积累量不到补充甘油细胞的10%。这些结果表明,在大肠杆菌缺乏磷脂合成的情况下,脂肪酸合成受到抑制。

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