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首页> 外文OA文献 >Cloning and sequencing of a Shiga-like toxin type II variant from Escherichia coli strain responsible for edema disease of swine.
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Cloning and sequencing of a Shiga-like toxin type II variant from Escherichia coli strain responsible for edema disease of swine.

机译：负责猪水肿病的大肠杆菌菌株的志贺样毒素II型变异体的克隆和测序。

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A Shiga-like toxin type II variant (SLT-IIv) is produced by strains of Escherichia coli responsible for edema disease of swine and is antigenically related to Shiga-like toxin type II (SLT-II) of enterohemorrhagic E. coli. However, SLT-IIv is only active against Vero cells, whereas SLT-II is active against both Vero and HeLa cells. The structural genes for SLT-IIv were cloned from E. coli S1191, and the nucleotide sequence was determined and compared with those of other members of the Shiga toxin family. The A subunit genes for SLT-IIv and SLT-II were highly homologous (94%), whereas the B subunit genes were less homologous (79%). The SLT-IIv genes were more distantly related (55 to 60% overall homology) to the genes for Shiga toxin of Shigella dysenteriae type 1 and the nearly identical Shiga-like toxin type I (SLT-I) of enterohemorrhagic E. coli. (These toxins are referred to together as Shiga toxin/SLT-I.) The A subunit of SLT-IIv, like those of other members of this toxin family, had regions of homology with the plant lectin ricin. SLT-IIv did not bind to galactose-alpha 1-4-galactose conjugated to bovine serum albumin, which is an analog of the eucaryotic cell receptor for Shiga toxin/SLT-I and SLT-II. These findings support the hypothesis that SLT-IIv binds to a different cellular receptor than do other members of the Shiga toxin family but has a similar mode of intracellular action. The organization of the SLT-IIv operon was similar to that of other members of the Shiga toxin family. Iron did not suppress SLT-IIv or SLT-II production, in contrast with its effect on Shiga toxin/SLT-I. Therefore, the regulation of synthesis of SLT-IIv and SLT-II differs from that of Shiga toxin/SLT-I.
机译：负责猪水肿病的大肠杆菌菌株产生了志贺样毒素II型变体（SLT-IIv），并且与肠出血性大肠杆菌的志贺样毒素II型（SLT-II）抗原相关。但是，SLT-IIv仅对Vero细胞具有活性，而SLT-II对Vero和HeLa细胞均具有活性。从大肠杆菌S1191克隆了SLT-IIv的结构基因，确定了核苷酸序列，并与志贺毒素家族的其他成员进行了比较。 SLT-IIv和SLT-II的A亚基基因高度同源（94％），而B亚基基因同源性较低（79％）。 SLT-IIv基因与痢疾志贺氏菌1型的志贺毒素基因和肠出血性大肠杆菌的几乎相同的志贺样毒素I型（SLT-1）的基因更远相关（总体同源性为55％至60％）。 （这些毒素一起称为志贺毒素/SLT-I。）SLT-IIv的A亚基，与该毒素家族其他成员的亚基一样，与植物凝集素蓖麻毒蛋白有同源性。 SLT-IIv不结合与牛血清白蛋白结合的半乳糖-α1-4-半乳糖，后者是志贺毒素/ SLT-I和SLT-II的真核细胞受体的类似物。这些发现支持以下假设：SLT-IIv与志贺毒素家族其他成员结合的细胞受体不同，但具有相似的细胞内作用模式。 SLT-IIv操纵子的组织类似于志贺毒素家族的其他成员。与铁对志贺毒素/ SLT-1的作用相反，铁没有抑制SLT-IIv或SLT-II的产生。因此，SLT-IIv和SLT-II的合成调控不同于志贺毒素/ SLT-1的调控。

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