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铁和温度对大肠杆菌产生志贺样毒素I的影响。

Effects of iron and temperature on Shiga-like toxin I production by Escherichia coli.

作者信息

Weinstein D L, Holmes R K, O'Brien A D

机构信息

Department of Microbiology, Uniformed Services University of the Health Sciences, Bethesda, Maryland 20814-4799.

出版信息

Infect Immun. 1988 Jan;56(1):106-11. doi: 10.1128/iai.56.1.106-111.1988.

DOI:10.1128/iai.56.1.106-111.1988
PMID:3121508
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC259242/
Abstract

Iron is known to depress Shiga toxin production by Shigella dysenteriae 1, and temperature has been shown to regulate several genes required for Shigella invasiveness. In this study, the influence of iron and temperature on regulation of a highly related toxin, Shiga-like toxin I (SLT-I) of enterohemorrhagic Escherichia coli, was examined in strains lysogenic for the toxin-converting coliphage 933J and in strains carrying the cloned slt-I genes on a high-copy-number plasmid vector. For comparison, S. dysenteriae 1 was included in these studies. As expected, iron suppressed Shiga toxin synthesis, and reduced growth temperature was also found to decrease Shiga toxin production. Iron also suppressed SLT-I synthesis in E. coli lysogenized with phage 933J but did not demonstrably repress toxin synthesis in E. coli strains carrying the cloned slt-I genes. Temperature had no effect on SLT-I synthesis. Mini-Mu lac operon fusions were then isolated in the cloned slt-I genes and used to test for regulation of beta-galactosidase by iron. Iron did not decrease beta-galactosidase production in strains that harbored these operon fusion plasmids. Taken together, these results indicate that iron but not temperature represses SLT-I synthesis when the slt-I genes are phage associated but this suppression is not easily demonstrated when the slt-I genes are cloned on a high-copy-number plasmid.

摘要

已知铁可抑制痢疾志贺氏菌1型产生志贺毒素,并且温度已被证明可调节志贺氏菌侵袭所需的几个基因。在本研究中,在携带毒素转化性大肠杆菌噬菌体933J的溶原性菌株以及在高拷贝数质粒载体上携带克隆的slt-I基因的菌株中,研究了铁和温度对肠出血性大肠杆菌高度相关毒素志贺样毒素I(SLT-I)调节的影响。为作比较,这些研究中纳入了痢疾志贺氏菌1型。正如预期的那样,铁抑制了志贺毒素的合成,并且还发现降低生长温度会减少志贺毒素的产生。铁也抑制了用噬菌体933J溶原化的大肠杆菌中SLT-I的合成,但在携带克隆的slt-I基因的大肠杆菌菌株中并未明显抑制毒素合成。温度对SLT-I的合成没有影响。然后在克隆的slt-I基因中分离出Mini-Mu lac操纵子融合体,并用于测试铁对β-半乳糖苷酶的调节作用。铁不会降低携带这些操纵子融合质粒的菌株中β-半乳糖苷酶的产生。综上所述,这些结果表明,当slt-I基因与噬菌体相关时,铁而非温度会抑制SLT-I的合成,但当slt-I基因克隆在高拷贝数质粒上时,这种抑制作用不易表现出来。

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