Dukan S, Dadon S, Smulski D R, Belkin S
J. Blaustein Desert Research Institute, Ben-Gurion University of the Negev, Israel.
Appl Environ Microbiol. 1996 Nov;62(11):4003-8. doi: 10.1128/aem.62.11.4003-4008.1996.
A series of plasmids, containing fusions of different stress promoters to lux reporter genes, was used in an attempt to monitor the defense circuits activated upon exposure of Escherichia coli to sublethal doses of free chlorine. A significant level of activation was exhibited by promoters of three heat shock genes (grpE, dnaK, and lon), in an rpoH-dependent manner. The promoter of micF, a gene under the control of the soxRS regulon, was also strongly induced, but not in a soxR mutant. This induction was not affected by sodA and sodB mutations, implying that it did not involve oxygen radical activity. Free-chlorine activation of both heat shock and soxRS regulons required an exposure of less then I s in duration. The oxyR or the SOS regulons were apparently not induced by free chlorine (as judged by lack of activation of katG and recA, respectively), and neither was the universal stress (uspA) protein.
一系列含有不同应激启动子与lux报告基因融合体的质粒被用于尝试监测大肠杆菌暴露于亚致死剂量游离氯时激活的防御回路。三个热休克基因(grpE、dnaK和lon)的启动子以rpoH依赖的方式表现出显著水平的激活。micF基因的启动子受soxRS调节子控制,也被强烈诱导,但在soxR突变体中未被诱导。这种诱导不受sodA和sodB突变的影响,这意味着它不涉及氧自由基活性。热休克和soxRS调节子的游离氯激活需要持续时间少于1秒的暴露。氧自由基调节子或SOS调节子显然未被游离氯诱导(分别通过katG和recA缺乏激活来判断),通用应激(uspA)蛋白也未被诱导。