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锰与抗生素生物合成。III. 荨麻青霉中锰对棒曲霉素产生的控制位点。

Manganese and antibiotic biosynthesis. III. The site of manganese control of patulin production in Penicillium urticae.

作者信息

Scott R E, Jones A, Gaucher G M

出版信息

Can J Microbiol. 1986 Mar;32(3):273-9. doi: 10.1139/m86-053.

Abstract

Although manganese had been shown to be an essential requirement for patulin biosynthesis, its site of action was unknown. Four possibilities were considered. A manganese requirement for the second pathway enzyme, a decarboxylase, was discounted since mid and late pathway intermediates were not converted to patulin in manganese-deficient cultures. A major disruption in primary metabolism and hence secondary metabolism was discounted since eight primary metabolism enzymes showed no evidence of unusual changes in specific activity when normal and manganese-deficient cultures were compared. Inhibitor studies using actinomycin D and cycloheximide showed that there was no activation of preexisting enzyme proteins and that manganese did not influence translation. The inhibitor studies did show, however, that manganese exercised its effect on patulin biosynthesis by influencing the coordinate appearance of pathway enzymes though an effect at the level of transcription.

摘要

尽管已证明锰是棒曲霉素生物合成的必需元素,但其作用位点尚不清楚。考虑了四种可能性。由于在缺锰培养物中,途径中期和后期的中间体未转化为棒曲霉素,因此排除了第二条途径的酶(一种脱羧酶)对锰的需求。由于比较正常培养物和缺锰培养物时,八种初级代谢酶的比活性没有显示出异常变化的迹象,因此排除了初级代谢进而次级代谢的重大破坏。使用放线菌素D和环己酰亚胺的抑制剂研究表明,不存在对预先存在的酶蛋白的激活作用,并且锰不影响翻译。然而,抑制剂研究确实表明,锰通过影响转录水平上途径酶的协同出现,对棒曲霉素生物合成发挥作用。

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