Nakajima Kenji
Laboratory of Biochemistry, Faculty of Nutrition, Koshien University, Takarazuka, Hyogo, Japan.
J Nutr Sci Vitaminol (Tokyo). 2005 Aug;51(4):271-3. doi: 10.3177/jnsv.51.271.
The regulatory mechanisms of riboflavin biosynthesis in the resting cells of a riboflavin-adenine-deficient mutant of Bacillus subtilis were examined. The growth and pH of the medium remained unchanged in spite of the administration of 0-200 microg/mL riboflavin to the medium during incubation of the resting cells for 17 h. However, the formation of 6,7-dimethyl-8-ribityllumazine (DMRL) and flavin adenine dinucleotide (FAD) was restricted and augmented and then reached its plateau, showing an inverse relation in the addition of riboflavin up to 50 microg/mL to the medium and a parallel relation in the supplementation of riboflavin up to 200 microg/mL to the medium. In the experiments, the amount of flavin mononucleotide (FMN) was negligible and riboflavin was not detected in the resting cells. The results indicated that not the repression of related enzymes but negative feedback inhibition by FAD, but not that by riboflavin or FMN, is operative in the biosynthetic pathway of riboflavin in the riboflavin adenine double-less mutant of Bacillus subtilis.
对枯草芽孢杆菌核黄素 - 腺嘌呤缺陷型突变体静止细胞中核黄素生物合成的调控机制进行了研究。在静止细胞培养17小时的过程中，尽管向培养基中添加了0 - 200微克/毫升的核黄素，但培养基的生长和pH值保持不变。然而，6,7 - 二甲基 - 8 - 核糖基 lumazine（DMRL）和黄素腺嘌呤二核苷酸（FAD）的形成受到限制，随后增加并达到平稳状态，在向培养基中添加高达50微克/毫升核黄素时呈现反比关系，在向培养基中添加高达200微克/毫升核黄素时呈现平行关系。在实验中，黄素单核苷酸（FMN）的量可忽略不计，并且在静止细胞中未检测到核黄素。结果表明，在枯草芽孢杆菌核黄素腺嘌呤双缺陷突变体的核黄素生物合成途径中，起作用的不是相关酶的阻遏，而是FAD的负反馈抑制，而非核黄素或FMN的负反馈抑制。
