Antonenka Uladzimir, Nölting Christina, Heesemann Jürgen, Rakin Alexander
Max von Pettenkofer-Institute of Hygiene and Medical Microbiology, Pettenkofer Str. 9a, D-80336 Munich, Germany.
Int J Med Microbiol. 2006 Oct;296(6):341-52. doi: 10.1016/j.ijmm.2006.02.021. Epub 2006 Jun 6.
Two genomic islands, namely the high-pathogenicity island (HPI) and Ecoc54N target the same asn tRNA genes to integrate into the bacterial chromosome. The HPI encodes the siderophore yersiniabactin in the highly pathogenic Yersinia group (Yersinia pestis, Yersinia pseudotuberculosis and Yersinia enterocolitica 1B) whilst the Ecoc54N island possibly encodes a polyketide synthase with an unknown function in the uropathogenic Escherichia coli CFT073 strain. HPI encodes the recombinase that promotes site-specific recombination (both integrative and excisive) with its corresponding attachment targets. A recombinase orthologue is also present in Ecoc54N. In addition, the HPI(Yps) of the Y. pestis/Y. pseudotuberculosis evolutionary lineage encodes the excisionase (recombination directionality factor, Xis(HPI)) that facilitates excision of the island. However, no sequence resembling the excisionase gene could be found in Ecoc54N. The rate of the HPI(Yps) excision estimated by real-time PCR was 10(-6) in Y. pseudotuberculosis. The presence of the excisionase increased the efficiency of the excisive recombination only eight fold. However, the introduction of the xis(HPI) in E. coli CFT073 did not influence the excision of Ecoc54N. The Xis(HPI) is encoded by the variable AT-rich part of the HPI(Yps) and substantially differs from its cognate recombinase in A+T content and codon usage. Also the Xis(HPI)-protected region, defined in the HPI attachment site, has suffered several nucleotide substitutions in Ecoc54N that could influence interaction with the excisionase. We propose that the pathogenicity islands (PAIs) targeting asn tRNA genes (PAIs(asn tRNA)) might have acquired recombinase and excisionase (HPI) genes independently and sequentially.
两个基因组岛,即高致病性岛(HPI)和Ecoc54N,靶向相同的天冬酰胺tRNA基因以整合到细菌染色体中。HPI在高致病性耶尔森菌属(鼠疫耶尔森菌、假结核耶尔森菌和小肠结肠炎耶尔森菌1B)中编码铁载体耶尔森菌素,而Ecoc54N岛可能在尿路致病性大肠杆菌CFT073菌株中编码一种功能未知的聚酮合酶。HPI编码促进与其相应附着靶点进行位点特异性重组(整合和切除)的重组酶。Ecoc54N中也存在重组酶同源物。此外,鼠疫耶尔森菌/假结核耶尔森菌进化谱系的HPI(Yps)编码促进该岛切除的切除酶(重组方向性因子,Xis(HPI))。然而,在Ecoc54N中未发现与切除酶基因相似的序列。通过实时PCR估计,假结核耶尔森菌中HPI(Yps)的切除率为10^(-6)。切除酶的存在仅将切除性重组的效率提高了8倍。然而,在大肠杆菌CFT073中引入xis(HPI)并不影响Ecoc54N的切除。Xis(HPI)由HPI(Yps)的富含AT的可变部分编码,其A+T含量和密码子使用情况与其同源重组酶有很大不同。同样,在HPI附着位点定义的Xis(HPI)保护区域在Ecoc54N中也发生了几次核苷酸替换,这可能会影响与切除酶的相互作用。我们提出,靶向天冬酰胺tRNA基因的致病岛(PAIs(asn tRNA))可能是独立且相继获得重组酶和切除酶(HPI)基因的。