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荚膜红细菌中参与钴胺素(维生素B12)合成后期步骤的基因的鉴定与序列分析。

Identification and sequence analysis of genes involved in late steps in cobalamin (vitamin B12) synthesis in Rhodobacter capsulatus.

作者信息

Pollich M, Klug G

机构信息

Institut für Mikro- und Molekularbiologie, Giessen, Germany.

出版信息

J Bacteriol. 1995 Aug;177(15):4481-7. doi: 10.1128/jb.177.15.4481-4487.1995.

DOI:10.1128/jb.177.15.4481-4487.1995
PMID:7635831
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC177200/
Abstract

A 6.4-kb region of a 6.8-kb BamHI fragment carrying Rhodobacter capsulatus genes involved in late steps of cobalamin synthesis has been sequenced. The nucleotide sequence and genetic analysis revealed that this fragment contains eight genes arranged in at least three operons. Five of these eight genes show homology to genes involved in the cobalamin synthesis of Pseudomonas denitrificans and Salmonella typhimurium. The arrangement of these homologous genes differs considerably in the three genera. Upstream of five overlapping genes (named bluFEDCB), a promoter activity could be detected by using lacZ fusions. This promoter shows no regulation by oxygen, vitamin B12 (cobalamin), or cobinamide. Disruption of the bluE gene by a Tn5 insertion (strain AH2) results in reduced expression of the puf and puc operons, which encode pigment-binding proteins of the photosynthetic apparatus. The mutant strain AH2 can be corrected to a wild-type-like phenotype by addition of vitamin B12 or cobinamide dicyanide. Disruption of the bluB gene by an interposon (strain BB1) also disturbs the formation of the photosynthetic apparatus. The mutation of strain BB1 can be corrected by vitamin B12 but not by cobinamide. We propose that a lack of cobalamin results in deregulation and a decreased formation of the photosynthetic apparatus.

摘要

对携带参与钴胺素合成后期步骤的荚膜红细菌基因的一个6.8 kb BamHI片段中的6.4 kb区域进行了测序。核苷酸序列和遗传分析表明,该片段包含至少三个操纵子中排列的八个基因。这八个基因中的五个与参与反硝化假单胞菌和鼠伤寒沙门氏菌钴胺素合成的基因具有同源性。这些同源基因在这三个属中的排列有很大差异。在五个重叠基因(命名为bluFEDCB)的上游,通过使用lacZ融合可以检测到启动子活性。该启动子不受氧气、维生素B12(钴胺素)或钴胺酰胺的调节。通过Tn5插入破坏bluE基因(菌株AH2)导致编码光合装置色素结合蛋白的puf和puc操纵子的表达降低。通过添加维生素B12或钴胺酰胺二氰化物可以将突变菌株AH2校正为野生型样表型。通过插入子破坏bluB基因(菌株BB1)也会干扰光合装置的形成。菌株BB1的突变可以通过维生素B12校正,但不能通过钴胺酰胺校正。我们提出,钴胺素的缺乏导致光合装置的失调和形成减少。

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