Mühldorfer I, Hacker J, Keusch G T, Acheson D W, Tschäpe H, Kane A V, Ritter A, Olschläger T, Donohue-Rolfe A
Lehrstuhl fäur Molekulare Infektionsbiologie, Universität Würzburg, Germany.
Infect Immun. 1996 Feb;64(2):495-502. doi: 10.1128/iai.64.2.495-502.1996.
Investigations of the regulation of the bacteriophage-encoded Shiga-like toxin II (SLT-II) in Escherichia coli demonstrated that bacteriophages exhibit a regulatory impact on toxin production by two mechanisms. Firstly, replication of the toxin-converting bacteriophages brings about an increase in toxin production due to concomitant multiplication of toxin gene copies. Secondly, an influence of a phage-encoded regulatory molecule was demonstrated by using low-copy-number plasmid pADR-28, carrying a translational gene fusion between the promoter and proximal portion of slt-IIA and the structural gene for bacterial alkaline phosphatase (phoA). PhoA activity, reflecting the slt-II promoter activity, was significantly enhanced in E. coli strains which and been lysogenized with an SLT-I or SLT-II-converting bacteriophage (H-19B or 933W, respectively) or bacteriophage lambda. Both mechanisms are dependent on bacteriophage induction and hence are recA dependent. Moreover, the study revealed that the DNA-binding protein H-NS has a regulatory impact on both bacteriophage-mediated SLT-II synthesis and the activity of the slt-II promoter of plasmid pADR-28. While a slight impact of growth temperature on SLT-II expression was observed, no impact of either osmolarity, pH, oxygen tension, acetates, iron level, or utilized carbon source could be demonstrated.
对大肠杆菌中噬菌体编码的志贺样毒素II(SLT-II)调控的研究表明,噬菌体通过两种机制对毒素产生具有调控作用。首先,毒素转化噬菌体的复制会导致毒素产生增加,这是由于毒素基因拷贝数随之增加。其次,通过使用低拷贝数质粒pADR-28证明了噬菌体编码的调控分子的影响,该质粒携带slt-IIA启动子和近端部分与细菌碱性磷酸酶(phoA)结构基因之间的翻译基因融合。反映slt-II启动子活性的PhoA活性在分别用SLT-I或SLT-II转化噬菌体(分别为H-19B或933W)或噬菌体λ溶原化的大肠杆菌菌株中显著增强。这两种机制都依赖于噬菌体诱导,因此依赖于recA。此外,研究表明DNA结合蛋白H-NS对噬菌体介导的SLT-II合成和质粒pADR-28的slt-II启动子活性都有调控作用。虽然观察到生长温度对SLT-II表达有轻微影响,但未证明渗透压、pH、氧张力、乙酸盐、铁水平或所用碳源对其有影响。