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首页> 外文期刊>Infection and immunity >The Cytotoxic Necrotizing Factors from Yersinia pseudotuberculosis and from Escherichia coli Bind to Different Cellular Receptors but Take the Same Route to the Cytosol
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The Cytotoxic Necrotizing Factors from Yersinia pseudotuberculosis and from Escherichia coli Bind to Different Cellular Receptors but Take the Same Route to the Cytosol

机译：假性耶尔森氏菌和大肠杆菌的细胞毒性坏死因子与不同的细胞受体结合，但通往细胞溶胶的途径相同

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摘要

The cytotoxic necrotizing factors CNF1 and CNF2 produced by pathogenic Escherichia coli strains and CNFY of Yersinia pseudotuberculosis constitutively activate small GTPases of the Rho family. They deamidate a glutamine (Gln63 in RhoA), which is crucial for GTP hydrolysis. CNF1 and CNFY exhibit 61% identity on the amino acid level, with equal distribution over the whole molecule. Although the two toxins are homologous in the receptor binding domain, we show that they bind to different cellular receptors. CNFY does not enter Caco-2 and CHO-K1 cells, which are responsive to CNF1. In contrast, HeLa, Hep-2, and HEK 293 cells do respond to both toxins. Competition studies with catalytically inactive mutants of the toxins revealed that binding of CNF1 has no influence on the uptake of CNFY into HeLa cells. In contrast, uptake of CNF1 is retarded after preincubation of HeLa cells with the catalytically inactive mutant of CNFY, suggesting that the toxin receptors overlap. Moreover, we compared the pathways of the toxins from receptor binding into the cytosol and showed that both toxins are taken up independent of the presence of clathrin or lipid rafts and are released into the cytosol from acidified endosomes.
机译：致病性大肠杆菌菌株产生的细胞毒性坏死因子CNF1和CNF2和假单胞菌耶尔森氏菌的CNF Y 组成性地激活了Rho家族的小GTP酶。他们使谷氨酰胺脱氨（RhoA中的Gln63），这对GTP水解至关重要。 CNF1和CNF Y 在氨基酸水平上具有61％的同一性，在整个分子上均等分布。尽管两种毒素在受体结合域中是同源的，但我们表明它们与不同的细胞受体结合。 CNF Y 不会进入对CNF1有反应的Caco-2和CHO-K1细胞。相反，HeLa，Hep-2和HEK 293细胞确实对两种毒素都有反应。对毒素的催化失活突变体的竞争研究表明，CNF1的结合对CNF Y 对HeLa细胞的摄取没有影响。相比之下，将HeLa细胞与CNF Y 的催化失活突变体预孵育后，CNF1的吸收受阻，表明毒素受体重叠。此外，我们比较了毒素从受体结合到细胞质中的途径，结果表明两种毒素的吸收都与网格蛋白或脂筏的存在无关，并从酸化的内体释放到细胞质中。

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