首页> 外文期刊>FEMS Microbiology Letters >Structural and functional analysis of the riboflavin synthesis genes encoding GTP cyclohydrolase II (ribA), DHBP synthase (ribBA), riboflavin synthase (ribC), and riboflavin deaminase/reductase (ribD) from Helicobacter pylori strain P1
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Structural and functional analysis of the riboflavin synthesis genes encoding GTP cyclohydrolase II (ribA), DHBP synthase (ribBA), riboflavin synthase (ribC), and riboflavin deaminase/reductase (ribD) from Helicobacter pylori strain P1

机译:幽门螺杆菌P1株编码GTP环水解酶II(ribA),DHBP合酶(ribBA),核黄素合酶(ribC)和核黄素脱氨酶/还原酶(ribD)的核黄素合成基因的结构和功能分析

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摘要

The functions of the riboflavin synthesis gene homologues ribA, ribBA, ribC, and ribD from Helicobacter pylori strain P1 were confirmed by complementation of defined Escherichia coli mutant strains. The H. pylori ribBA gene, which is similar to bifunctional ribBA genes of Gram-positive bacteria, fully complemented the ribB mutation and partially restored growth in a ribC mutant. However, ribBA did not complement the ribA mutation in E. coli, thus explaining the presence of the additional separate copy of the ribA gene in the H. pylori chromosome. In E. coli exclusively ribA conferred hemolytic activity and gave rise to production of molecules with fluorescence characteristics similar to flavins, as observed earlier. The E. coli hemolysin ClyA was not involved in causing the hemolytic phenotype. No riboflavin synthesis genes on plasmids conferred iron uptake functions to a siderophore-deficient mutant of E. coli. Marker exchange mutagenesis of the genes in H. pylori was not successful indicating that riboflavin synthesis is essential for basic metabolic functions of the gastric pathogen. (C) 2000 Federation of European Microbiological Societies. Published by Elsevier Science B.V. All rights reserved. [References: 18]
机译:幽门螺杆菌菌株P1的核黄素合成基因同源物ribA,ribBA,ribC和ribD的功能通过确定的大肠杆菌突变菌株的互补得到证实。幽门螺杆菌ribBA基因与革兰氏阳性细菌的双功能ribBA基因相似,完全补充了ribB突变并部分恢复了ribC突变体的生长。但是,ribBA不能补充大肠杆菌中的ribA突变,因此可以解释幽门螺杆菌染色体中存在另外的ribA基因单独拷贝。如前所述,在大肠杆菌中,ribA仅赋予溶血活性,并产生具有类似于黄素的荧光特征的分子。大肠杆菌溶血素ClyA不参与引起溶血表型。质粒上没有核黄素合成基因将铁的摄取功能赋予大肠杆菌铁载体不足的突变体。幽门螺杆菌中基因的标记交换诱变不成功,表明核黄素合成对于胃病原体的基本代谢功能至关重要。 (C)2000年欧洲微生物学会联合会。由Elsevier Science B.V.保留所有权利。 [参考:18]

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