Construction of deletion mutants of Shiga (-like) toxin genes (stx-1 and/or stx-2) on enterohemorrhagic Escherichia coli (O157: H7)

被引：0

作者：

Yokoyama, S

Suzuki, T

Shiraishi, S

Ohishi, N

Yagi, K

Ichihara, S

Itoh, S

Mori, H

机构：

[1] Gifu Pharmaceut Univ, Dept Publ Hlth Pharm, Microbiol Lab, Gifu 5028585, Japan

[2] Gifu Univ, Fac Agr, Dept Biotechnol, Gifu 5011193, Japan

[3] Inst Appl Biochem, Gifu 5050116, Japan

[4] Gifu Int Inst Biotechnol, Gifu 5050116, Japan

[5] Meijo Univ, Fac Agr, Microbiol Lab, Nagoya, Aichi 4688502, Japan

来源：

JOURNAL OF CLINICAL BIOCHEMISTRY AND NUTRITION | 2001年 / 30卷

关键词：

Shiga (-like) toxin; deletion mutants; enterohemorrhagic; Escherichia coli; O157 : H7;

D O I：

暂无

中图分类号：

R15 [营养卫生、食品卫生]; TS201 [基础科学];

学科分类号：

100403 ;

摘要：

We constructed isogenic Shiga (-like) toxin (Stx-1 and/or Stx-2) gene-deletion mutants of enterohemorrhagic Escherichia coli (EHEC) GPU96MM (O157: H7). A vector with temperature-sensitive replication origin was used for the construction. The parts of stx-1 and stx-2 on the GPU96MM genome were replaced with kanamycin and chloramphenicol resistance genes, respectively. The mutants deficient in stx-1, stx-2, and both of them were named GPU993, GPU994, and GPU995, respectively. Each mutation was, confirmed by the polymerase chain reaction, enzyme-linked immunosorbent assay using antibodies to B subunits of Stx-1 and Stx-2, and the cytotoxic activity of the bacterial culture supernatants toward HeLa cells was detected for GPU96MM and the mutants except for GPU995. These results indicate that GPU993 and GPU994 lack productivity for the respective toxins and GPU995, for both of them.

引用

页码：33 / 42

页数：10

共 18 条

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