Clark D
J Bacteriol. 1981 Nov;148(2):521-6. doi: 10.1128/jb.148.2.521-526.1981.
Fusion of the lacZ gene coding for beta-galactosidase to the fadA,B and fadE operons was accomplished by using the phage Mu d (Apr lac). In such fusion strains, beta-galactosidase was induced by long-chain fatty acids and repressed by glucose, as is the normal pattern of control for the enzymes of the fad regulon. The level of induction seen was approximately 10-fold for both the fadA and fadE operons. These results demonstrate that the previously observed regulation of both the fadA and fadE operons is at the transcriptional level. When an insertion mutation in the fadR (repressor) gene was introduced into the fusion strains, beta-galactosidase was produced constitutively. A series of fatty acids of different chain lengths were tested as inducers. Acids of chain lengths of 10 carbon atoms or less failed to induce, those of 12 carbon atoms induced partly, and those of 14 or more carbon atoms induced fully. Imidazole was found to counteract the glucose repression of the fadA operon as recently demonstrated for the ara operon.
通过使用噬菌体Mu d(Apr lac),实现了将编码β-半乳糖苷酶的lacZ基因与fadA、B和fadE操纵子融合。在这种融合菌株中,β-半乳糖苷酶由长链脂肪酸诱导,并被葡萄糖抑制,这与fad调节子中酶的正常调控模式相同。对于fadA和fadE操纵子,观察到的诱导水平约为10倍。这些结果表明,先前观察到的fadA和fadE操纵子的调控是在转录水平上。当将fadR(阻遏物)基因中的插入突变引入融合菌株时,β-半乳糖苷酶组成型产生。测试了一系列不同链长的脂肪酸作为诱导剂。10个碳原子或更少碳原子链长的酸不能诱导,12个碳原子链长的酸部分诱导,14个或更多碳原子链长的酸完全诱导。发现咪唑可以抵消fadA操纵子的葡萄糖抑制作用,这与最近对ara操纵子的证明相同。