Heimer Susan R, Welch Rod A, Perna Nicole T, Pósfai György, Evans Peter S, Kaper James B, Blattner Fred R, Mobley Harry L T
Department of Microbiology and Immunology, University of Maryland School of Medicine, Baltimore, Maryland 21201, USA.
Infect Immun. 2002 Feb;70(2):1027-31. doi: 10.1128/IAI.70.2.1027-1031.2002.
Recent genomic analyses of Escherichia coli O157:H7 strain EDL933 revealed two loci encoding urease gene homologues (ureDABCEFG), which are absent in nonpathogenic E. coli strain K-12. This report demonstrates that the cloned EDL933 ure gene cluster is capable of synthesizing urease in an E. coli DH5alpha background. However, when the gene fragment is transformed back into the native EDL933 background, the enzymatic activity of the cloned determinants is undetectable. We speculate that an unidentified trans-acting factor in enterohemorrhagic E. coli (EHEC) is responsible for this regulation of ure expression. In addition, Fur-like recognition sites are present in three independent O157:H7 isolates upstream of ureD and ureA. Enzymatic assays confirmed a difference in urease expression of cloned EHEC ure clusters in E. coli MC3100Deltafur. Likewise, interruption of fur in O157:H7 isolate IN1 significantly diminished urease activity. We propose that, similar to the function of Fur in regulating the acid response of Salmonella enterica serovar Typhimurium, it modulates urease expression in EHEC, perhaps contributing to the acid tolerance of the organism.
最近对大肠杆菌O157:H7菌株EDL933的基因组分析显示，有两个位点编码脲酶基因同源物（ureDABCEFG），而在非致病性大肠杆菌K-12菌株中不存在这些位点。本报告表明，克隆的EDL933脲酶基因簇能够在大肠杆菌DH5α背景中合成脲酶。然而，当该基因片段转化回天然的EDL933背景时，克隆的决定簇的酶活性无法检测到。我们推测，肠出血性大肠杆菌（EHEC）中一种未知的反式作用因子负责这种脲酶表达的调控。此外，在ureD和ureA上游的三个独立的O157:H7分离株中存在类Fur识别位点。酶活性测定证实了在大肠杆菌MC3100Deltafur中克隆的EHEC脲酶基因簇的脲酶表达存在差异。同样，O157:H7分离株IN1中fur的中断显著降低了脲酶活性。我们提出，与Fur在调节鼠伤寒沙门氏菌酸反应中的功能类似，它调节EHEC中的脲酶表达，可能有助于该生物体的耐酸性。
