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pColV - K30的气杆菌素操纵子的顺反子间区域的组织方式可能解释了iucABCD和iutA基因的差异表达。

The organization of intercistronic regions of the aerobactin operon of pColV-K30 may account for the differential expression of the iucABCD iutA genes.

作者信息

Martínez J L, Herrero M, de Lorenzo V

机构信息

Centro de Investigaciones Biológicas (C.S.I.C.), Madrid, Spain.

出版信息

J Mol Biol. 1994 Apr 29;238(2):288-93. doi: 10.1006/jmbi.1994.1290.

DOI:10.1006/jmbi.1994.1290
PMID:8003107
Abstract

The complete nucleotide sequence of the 8.3 kilobase operon of the enterobacterial virulence plasmid pColV-K30, which encodes a high-affinity iron transport system mediated by the hydroxamate siderophore aerobactin, has been determined. The region includes five open reading frames which correspond to the genes iucA, iucB, iucC and iucD, encoding the enzymes of the biosynthetic pathway for aerobactin, and iutA for the outer membrane receptor of ferri-aerobactin complexes. The sequences of the iucABCD genes are tightly coupled without any intervening non-coding sequence. The predicted secondary mRNA structures at the gene junctions within the iucABCD cluster, along with their codon usage, may account for the differential expression of each of the protein products, as observed in vivo with minicells. The genes iucA and iucC, which determine the two subunits of the aerobactin synthetase complex, showed a considerable homology within three stretches of their amino acid sequence. A potential operator sequence (iron box) for the binding of the iron(II)-responsive Fur repressor protein was found within the iucA coding region, suggesting that the operon is subjected to an additional level of transcriptional repression by iron (II).

摘要

编码由异羟肟酸铁载体气杆菌素介导的高亲和力铁转运系统的肠道细菌毒力质粒pColV-K30的8.3千碱基操纵子的完整核苷酸序列已被确定。该区域包括五个开放阅读框,分别对应于编码气杆菌素生物合成途径中酶的iucA、iucB、iucC和iucD基因,以及铁-气杆菌素复合物外膜受体的iutA基因。iucABCD基因的序列紧密相连,没有任何中间非编码序列。iucABCD簇内基因连接处预测的二级mRNA结构及其密码子使用情况,可能解释了每种蛋白质产物的差异表达,这在体内用微小细胞观察到。决定气杆菌素合成酶复合物两个亚基的iucA和iucC基因,在其氨基酸序列的三个区域内显示出相当大的同源性。在iucA编码区内发现了一个潜在的用于结合铁(II)响应性Fur阻遏蛋白的操纵序列(铁盒),这表明该操纵子受到铁(II)的额外转录抑制水平的调控。

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