Ralph E T, Guest J R, Green J
The Krebs Institute, Department of Molecular Biology and Biotechnology, University of Sheffield, Sheffield, S10 2TN, United Kingdom.
Proc Natl Acad Sci U S A. 1998 Sep 1;95(18):10449-52. doi: 10.1073/pnas.95.18.10449.
The recent outbreaks of Escherichia coli O157-associated food poisoning have focused attention on the virulence determinants of E. coli. Here, it is reported that single base substitutions in the fnr gene encoding the oxygen-responsive transcription regulator FNR (fumarate and nitrate reduction regulator) are sufficient to confer a hemolytic phenotype on E. coli K12, the widely used laboratory strain. The mechanism involves enhancing the expression of a normally dormant hemolysin gene (hlyE) located in the E. coli chromosome. The mutations direct single amino acid substitutions in the activating regions (AR1 and AR3) of FNR that contact RNA polymerase. It is concluded that altering a resident transcription regulator, or acquisition of a competent heterologous regulator, could generate a pool of hemolytic, and therefore more virulent, strains of E. coli in nature.
近期爆发的与大肠杆菌O157相关的食物中毒事件,使人们将注意力集中在了大肠杆菌的毒力决定因素上。在此报道,编码氧响应转录调节因子FNR(延胡索酸和硝酸盐还原调节因子)的fnr基因中的单碱基替换足以赋予广泛使用的实验室菌株大肠杆菌K12溶血表型。其机制涉及增强位于大肠杆菌染色体上一个通常处于休眠状态的溶血素基因(hlyE)的表达。这些突变导致FNR的激活区域(AR1和AR3)中与RNA聚合酶接触的单个氨基酸发生替换。得出的结论是,改变一个常驻转录调节因子,或获得一个有活性的异源调节因子,可能在自然界中产生一批具有溶血能力、因而更具毒性的大肠杆菌菌株。