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对幽门螺杆菌菌株P1中编码GTP环化水解酶II(ribA)、二氢生物蝶呤合酶(ribBA)、核黄素合酶(ribC)和核黄素脱氨酶/还原酶(ribD)的核黄素合成基因进行的结构和功能分析。

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.

作者信息

Fassbinder F, Kist M, Bereswill S

机构信息

University of Freiburg, Institute of Medical Microbiology and Hygiene, Department of Microbiology, Freiburg, Germany.

出版信息

FEMS Microbiol Lett. 2000 Oct 15;191(2):191-7. doi: 10.1111/j.1574-6968.2000.tb09339.x.

DOI:10.1111/j.1574-6968.2000.tb09339.x
PMID:11024263
Abstract

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.

摘要

通过对特定大肠杆菌突变株的互补作用,证实了幽门螺杆菌P1菌株中核黄素合成基因同源物ribA、ribBA、ribC和ribD的功能。幽门螺杆菌的ribBA基因与革兰氏阳性菌的双功能ribBA基因相似,完全互补了ribB突变,并部分恢复了ribC突变体中的生长。然而,ribBA不能互补大肠杆菌中的ribA突变,这就解释了幽门螺杆菌染色体中存在额外单独的ribA基因拷贝的原因。在大肠杆菌中,如先前观察到的那样,只有ribA具有溶血活性,并产生具有类似于黄素荧光特性的分子。大肠杆菌溶血素ClyA不参与引起溶血表型。质粒上的核黄素合成基因没有赋予缺铁载体的大肠杆菌突变体铁摄取功能。幽门螺杆菌中这些基因的标记交换诱变未成功,表明核黄素合成对于这种胃部病原体的基本代谢功能至关重要。

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