Urinary tract infections are one of the most common bacterial infections and a major public health problem. The predominant causative agents are uropathogenic Escherichia coli. These strains differ from commensal E. coli by the presence of additional horizontally acquired chromosomal material, so-called pathogenicity islands, which encode traits that promote efficient bacterial colonization of the urinary tract. Uropathogenic model strain E. coli 536 possesses six archetypal pathogenicity islands. Bacteriophage-like integrases encoded by each pathogenicity island contribute to island instability. To learn more about the stability of these six islands and factors controlling their stability we constructed two chromosomal reporter systems for the measurement of island loss, as well as for the measurement of the promoter activity of the six island-associated integrase genes at the population level. We used these reporter gene modules to analyze the role of SOS response in island instability. Tests with subinhibitory concentrations of different antibiotics, including many drugs commonly used for the treatment of urinary tract infection, indicated that only SOS response-inducing antibiotics led to an increased loss of islands which was always associated with an increase in the bacterial subpopulations showing high integrase promoter activity. This suggests that island excision correlates with the expression of the cognate integrase. Our reporter modules are valuable tools to investigate the impact of various growth conditions on genome plasticity. Furthermore, a better understanding of the conditions, which affect bacterial integrase expression may open ways to specifically manipulate the genome content of bacterial pathogens by increasing pathogenicity island deletion rates in infecting or colonizing bacteria, thus leading to the attenuation of bacterial pathogens.

尿路感染是最常见的细菌感染之一，也是主要的公共卫生问题。主要的病原体是尿路致病性大肠杆菌。这些菌株与共生大肠杆菌不同，因为存在其他水平获得的染色体物质，即所谓的致病岛，其编码促进尿道有效细菌定殖的性状。致病性模型菌株大肠杆菌536个拥有六个原型致病岛。由每个致病岛编码的噬菌体样整合有助于岛的不稳定。要了解有关这六个岛的稳定性以及控制其稳定性的因素的更多信息，我们构建了两个染色体报告系统，用于测量岛损失以及在种群水平上测量六个与岛相关的整合酶基因的启动子活性。我们使用这些报告基因模块来分析SOS应答在岛屿不稳定中的作用。亚抑制浓度的不同抗生素的测试，包括许多通常用于治疗尿路感染的药物，指出仅诱导SOS反应的抗生素导致孤岛损失增加，这总是与显示高整合酶启动子活性的细菌亚群的增加有关。这表明岛屿切除与同源整合酶的表达相关。我们的报告模块是研究各种生长条件对基因组可塑性影响的有价值的工具。此外，对影响细菌整合酶表达的条件的更好理解可能为通过增加感染或定居细菌的致病性岛缺失率从而特异性地控制细菌病原体的基因组含量开辟途径，从而导致细菌病原体的衰减。这表明岛屿切除与同源整合酶的表达相关。我们的报告模块是研究各种生长条件对基因组可塑性影响的有价值的工具。此外，对影响细菌整合酶表达的条件的更好理解可以为通过增加在感染或定殖细菌中的致病性岛缺失率从而特异性地控制细菌病原体的基因组含量开辟途径，从而导致细菌病原体的衰减。这表明岛屿切除与同源整合酶的表达相关。我们的报告模块是研究各种生长条件对基因组可塑性影响的有价值的工具。此外，对影响细菌整合酶表达的条件的更好理解可能为通过增加感染或定居细菌的致病性岛缺失率从而特异性地控制细菌病原体的基因组含量开辟途径，从而导致细菌病原体的衰减。