Jacques N A, Hunt A l
Biochim Biophys Acta. 1980 Sep 8;619(3):453-70. doi: 10.1016/0005-2760(80)90098-3.
The cyclopropane fatty acid, methylene hexadecanoic acid, constituted from 1% to upwards of 30% of the total lipid fatty acids of the bacterium, Pseudomonas denitrificans. The amount of this component varied along with the levels of the enzyme, cyclopropane synthetase (unsaturated-phospholipid methyltransferase, EC 2.1.1.16). When P. denitrificans was grown on succinate in a culture medium saturated with oxygen, cyclopropane synthetase remained repressed while cell densities were low. As cell densities increased, the enzyme was induced and the activity rose to a maximum over a period of 4-6 h. Cyclopropane synthetase could also be induced by rapidly limiting the oxygen supply to cells growing in conditions where oxygen was in excess. This phenomenon was independent of the phase of growth and could be prevented by addition of chloramphenicol to the medium. Growth on glucose was also shown to repress the synthesis of cyclopropane synthetase under similar conditions. However, once maximum levels of cyclopropane synthetase were reached, they remained constant for at least the following 15 h irrespective of the source of carbon in the medium. Methylene hexadecanoic acid accumulated in a linear manner throughout this period until a maximum level was achieved, the rate of accumulation being related to the activity of cyclopropane synthetase detected in vitro. The rate of conversion of total fatty acid to methylene hexadecanoic acid was approximately 1.3-1.5% per h, the methylene hexadecanoic acid being metabolically stable - the relative percentage of methylene hexadecanoic acid to total fatty acid in repressed cells, falling linearly with increase in cell number. Repression of enzyme synthesis was further investigated by growing cells on various sources of carbon other than glucose. The results indicated that succinate was unique amongst tricarboxylic acid cycle intermediates in depressing cyclopropane synthetase under limited oxygen conditions.
环丙烷脂肪酸，即亚甲基十六烷酸，在反硝化假单胞菌的总脂质脂肪酸中占比1%至30%以上。该成分的含量随环丙烷合成酶（不饱和磷脂甲基转移酶，EC 2.1.1.16）的水平而变化。当反硝化假单胞菌在饱和氧气的培养基中以琥珀酸为碳源生长时，在细胞密度较低时，环丙烷合成酶仍受到抑制。随着细胞密度增加，该酶被诱导，其活性在4 - 6小时内升至最高。对于在氧气过量条件下生长的细胞，通过迅速限制氧气供应也可诱导环丙烷合成酶。这种现象与生长阶段无关，并且可通过向培养基中添加氯霉素来阻止。在类似条件下，以葡萄糖为碳源生长也会抑制环丙烷合成酶的合成。然而，一旦环丙烷合成酶达到最高水平，无论培养基中的碳源如何，在至少接下来的15小时内其水平保持恒定。在此期间，亚甲基十六烷酸以线性方式积累，直至达到最高水平，积累速率与体外检测到的环丙烷合成酶活性相关。总脂肪酸向亚甲基十六烷酸的转化速率约为每小时1.3 - 1.5%，亚甲基十六烷酸在代谢上是稳定的——在受抑制的细胞中，亚甲基十六烷酸占总脂肪酸的相对百分比随细胞数量增加呈线性下降。通过让细胞在除葡萄糖以外的各种碳源上生长，进一步研究了酶合成的抑制作用。结果表明，在有限氧气条件下，琥珀酸在三羧酸循环中间体中是独特的，它能抑制环丙烷合成酶。
