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Production of Nucleic Acid-Related Substances by Fermentation Processes XXXIII. Accumulation of Inosine by a Mutant of Brevibacterium ammoniagenes

机译:通过发酵工艺XXXIII生产核酸相关物质。产氨短杆菌突变体对肌苷的积累

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Inosine-producing cultures were found among mutants resistant to 6-mercaptoguanine (6MG) derived from a 5′-inosinic acid (IMP)-producing strain, KY 13102, of Brevibacterium ammoniagenes. Inosine-producing ability was very frequent among the mutants resistant to a low concentration (10 to 50 μg/ml) of 6MG. The accumulation of inosine by strain KY 13714 was stimulated by a low concentration of adenine (25 mg/liter) but was depressed by high levels of adenine. The accumulation by strain KY 13714 was not inhibited by manganese ion but instead was stimulated by its excess, in contrast to IMP accumulation by KY 13102. Addition of hypoxanthine at an early stage of cultivation accelerated inosine accumulation. Furthermore, on addition of hypoxanthine and of a surface-activating agent after 48 hr of cultivation, the simultaneous accumulation of IMP and inosine was observed. A 9.3-mg amount of inosine per ml accumulated after 4 days of cultivation at 30 C. The inosine-producing mutant did not differ from the IMP-producing strain either in 5′ purine nucleotide degradation or in IMP formation from hypoxanthine. However, it was found to be completely devoid of purine nucleoside-degrading activity. The conversion of IMP accumulation to inosine can be explained by the lack of nucleosidedegrading activity. The relationship between deficiency of nucleoside-degrading activity and resistance to low levels of 6MG is discussed, and a new mechanism for 6MG resistance is presented.
机译:在衍生自产生氨气短杆菌的5'-肌苷酸(IMP)菌株KY 13102的6-巯基鸟嘌呤(6MG)耐药的突变体中发现了肌苷生成培养物。在对6MG的低浓度(10至50μg/ ml)具有抗性的突变体中,肌苷产生能力非常频繁。低浓度的腺嘌呤(25 mg / L)刺激了菌株KY 13714的肌苷积累,但高水平的腺嘌呤抑制了肌苷的积累。与KY 13102的IMP积累相反,菌株KY 13714的积累不受锰离子的抑制,而是受到锰离子的过量刺激。在培养的早期添加次黄嘌呤可加速肌苷的积累。此外,在培养48小时后添加次黄嘌呤和表面活化剂,观察到IMP和肌苷同时积累。在30°C下培养4天后,每毫升累积了9.3 mg肌苷。在5'嘌呤核苷酸降解或从次黄嘌呤形成IMP方面,产生肌苷的突变体与产生IMP的菌株没有区别。然而,发现它完全没有嘌呤核苷降解活性。 IMP积累向肌苷的转化可以通过缺乏核苷降解活性来解释。讨论了核苷降解活性不足与对低水平6MG的抗性之间的关系,并提出了6MG抗性的新机制。

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