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首页> 外文期刊>Infection and immunity >Molecular Characterization of a Glucose-Inhibited Division Gene, gidA, That Regulates Cytotoxic Enterotoxin of Aeromonas hydrophila
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Molecular Characterization of a Glucose-Inhibited Division Gene, gidA, That Regulates Cytotoxic Enterotoxin of Aeromonas hydrophila

机译：葡萄糖抑制分区基因，gidA，调节嗜水气单胞菌的细胞毒性肠毒素的分子表征。

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By using a mini-transposon, we obtained two mutated strains of a diarrheal isolate, SSU, of Aeromonas hydrophila that exhibited a 50 to 53% reduction in the hemolytic activity and 83 to 87% less cytotoxic activity associated with the cytotoxic enterotoxin (Act). Act is a potent virulence factor of A. hydrophila and has been shown to contribute significantly to the development of both diarrhea and septicemia in animal models. Subsequent cloning and DNA sequence analysis revealed that transposon insertion occurred at different locations in these two mutants within the same 1,890-bp open reading frame for the glucose-inhibited division gene (gidA). A similar reduction in hemolytic (46%) and cytotoxic (81%) activity of Act was noted in the gidA isogenic mutant of A. hydrophila that was generated by marker exchange mutagenesis. Northern blot analysis revealed that the transcription of the cytotoxic enterotoxin gene (act) was not altered in the gidA transposon and isogenic mutants. However, by generating a chromosomal act::alkaline phosphatase gene (phoA) reporter construct, we demonstrated significantly reduced phosphatase activity in these mutants, indicating the effect of glucose-inhibited division (GidA) protein in modulating act gene expression at the translational level. The biological effects of Act in the gidA mutants were restored by complementation. The virulence of the gidA mutants in mice was dramatically reduced compared to the those of the wild-type (WT) and complemented strains of A. hydrophila. The histopathological examination of lungs, in particular, indicated severe congestion, alveolar hemorrhage, and acute inflammatory infiltrate in the interstitial compartment and the alveolar spaces when mice were infected with the WT and complemented strains. Minimal-to-mild changes were noted in the lungs with the gidA mutants. Taken together, our data indicate for the first time that GidA regulates the most-potent virulence factor of A. hydrophila, Act.
机译：通过使用微型转座子，我们获得了两个突变的嗜水气单胞菌腹泻分离株SSU，其溶血活性降低了50％至53％，而与之相关的细胞毒活性降低了83％至87％与细胞毒性肠毒素（Act）。行为是 A的强大毒力因子。亲水性，并已证明在动物模型中对腹泻和败血病的发展有重大贡献。随后的克隆和DNA序列分析表明，转座子插入发生在葡萄糖抑制分裂基因（ gidA ）的同一1,890-bp开放阅读框中的这两个突变体的不同位置。在 A的 gidA 等基因突变体中，Act的溶血（46％）和细胞毒性（81％）活性降低了类似的程度。标记交换诱变产生的亲水性。 Northern印迹分析表明，在 gidA 转座子和同基因突变体中，细胞毒性肠毒素基因（ act ）的转录没有改变。然而，通过生成染色体 act ::碱性磷酸酶基因（ phoA ）报告基因构建体，我们证明了这些突变体中的磷酸酶活性显着降低，表明葡萄糖抑制分裂的作用（GidA）蛋白在翻译水平上调控 act 基因表达。通过互补，使Act在 gidA 突变体中的生物学效应得以恢复。与野生型（WT）和互补株的 A相比， gidA 突变体在小鼠中的毒性大大降低。亲水。特别是肺的组织病理学检查表明，当小鼠感染了WT和互补株后，严重的充血，肺泡出血和间质腔和肺泡间隙中的急性炎症浸润。在肺中， gidA 突变体的变化微乎其微。两者合计，我们的数据首次表明GidA调节 A最有效的毒力因子。亲水法。

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