首页> 美国卫生研究院文献>Antimicrobial Agents and Chemotherapy >Isolation of streptomycin-nonproducing mutants deficient in biosynthesis of the streptidine moiety or linkage between streptidine 6-phosphate and dihydrostreptose.
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Isolation of streptomycin-nonproducing mutants deficient in biosynthesis of the streptidine moiety or linkage between streptidine 6-phosphate and dihydrostreptose.

机译:分离链霉素部分生物合成不足的链霉素不产生突变体或链磷酸6-磷酸酯与二氢链糖之间的键合不足。

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摘要

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.
机译:通过紫外线诱变从灰链霉菌ATCC 10137中衍生出需要链霉素产生链霉素的八个链烷特异营养型突变体(SD20,SD81,SD141,SD189,SD245,SD261,SD263和SD274)。通过特异营养体积累的中间体的表征和链霉菌素生物合成中涉及的酶的分析,推断出该突变体的生化损伤如下:SD20和SD263,氨基转移; SD81,SD261和SD274磷酸化; SD141,氨基转移; SD189,脱氢; SD245,链磷酸6-磷酸酯和二氢链糖之间的连接。在SD245中发现了6-磷酸链烷烃的积累,削弱了其氨基转移酶的活性。这一发现表明氨基转移酶的活性可能已被链烷生物合成途径的终产物链磷酸6-磷酸链酯负控制。

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