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分离在链霉胍部分生物合成或磷酸链霉胍与二氢链霉糖之间的连接方面存在缺陷的不产生链霉素的突变体。

Isolation of streptomycin-nonproducing mutants deficient in biosynthesis of the streptidine moiety or linkage between streptidine 6-phosphate and dihydrostreptose.

作者信息

Ohnuki T, Imanaka T, Aiba S

出版信息

Antimicrob Agents Chemother. 1985 Mar;27(3):367-74. doi: 10.1128/AAC.27.3.367.

Abstract

Eight streptidine idiotrophic mutants (SD20, SD81, SD141, SD189, SD245, SD261, SD263, and SD274) which required streptidine to produce streptomycin were derived from Streptomyces griseus ATCC 10137 by UV mutagenesis. By both the characterization of intermediates accumulated by the idiotrophs and the assay of enzymes involved in streptidine biosynthesis, the biochemical lesions of the mutants were deduced as follows: SD20 and SD263, transamination; SD81, SD261, and SD274, phosphorylation; SD141, transamidination; SD189, dehydrogenation; SD245, linkage between streptidine 6-phosphate and dihydrostreptose. An accumulation of streptidine 6-phosphate was found in SD245 to impair its aminotransferase activity. This finding suggests that aminotransferase activity might have been negatively controlled by the end product, streptidine 6-phosphate, of the streptidine biosynthetic pathway.

摘要

通过紫外线诱变从灰色链霉菌ATCC 10137获得了八个对链霉胍营养缺陷的突变体(SD20、SD81、SD141、SD189、SD245、SD261、SD263和SD274),这些突变体需要链霉胍来产生链霉素。通过对营养缺陷型积累的中间体进行表征以及对链霉胍生物合成中涉及的酶进行测定,推断出突变体的生化损伤如下:SD20和SD263,转氨作用;SD81、SD261和SD274,磷酸化作用;SD141,转脒基作用;SD189,脱氢作用;SD245,链霉胍6-磷酸与二氢链霉糖之间的连接。在SD245中发现链霉胍6-磷酸的积累会损害其转氨酶活性。这一发现表明,转氨酶活性可能受到链霉胍生物合成途径的终产物链霉胍6-磷酸的负调控。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d07a/176279/fba26249f428/aac00181-0114-a.jpg

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