Odakura Y, Kase H, Nakayama K
J Antibiot (Tokyo). 1983 Feb;36(2):125-30. doi: 10.7164/antibiotics.36.125.
Production of sagamicin and gentamicin C1 in Micromonospora sagamiensis was regulated by cobalt ion. In a parental strain, KY11510, cobalt ion stimulated gentamicin C1 production and suppressed sagamicin production. By ultraviolet light or N-methyl-N'-nitro-N-nitrosoguanidine treatment, six mutants blocked in gentamicin C1 biosynthesis were obtained from KY11510. These mutants were classified into two types. The first type, four mutants, produced no gentamicin C1 even when cobalt ion was added to the fermentation. The second type, two mutants, produced a small amount of gentamicin C1 when a high concentration of cobalt ion was added. Based on biotransformation experiments, these mutants appeared to be blocked at the 6'-C-methylation step in the biosynthesis of gentamicin C1. The mutants showed an increased production of sagamicin. In addition, cobalt ion stimulated sagamicin production in the mutants. The mechanism of cobalt regulation in the parent and the mutants is discussed.
相模湾小单孢菌中相模霉素和庆大霉素C1的产生受钴离子调控。在亲本菌株KY11510中，钴离子刺激庆大霉素C1的产生并抑制相模霉素的产生。通过紫外线或N-甲基-N'-硝基-N-亚硝基胍处理，从KY11510中获得了6个在庆大霉素C1生物合成中受阻的突变体。这些突变体分为两种类型。第一种类型，4个突变体，即使在发酵中添加钴离子也不产生庆大霉素C1。第二种类型，2个突变体，当添加高浓度钴离子时产生少量庆大霉素C1。基于生物转化实验，这些突变体似乎在庆大霉素C1生物合成的6'-C-甲基化步骤受阻。这些突变体相模霉素的产量增加。此外，钴离子刺激突变体中相模霉素的产生。讨论了亲本和突变体中钴调控的机制。
