@article{mbs:/content/journal/micro/10.1099/mic.0.2006/003202-0, author = "Brzostek, Katarzyna and Brzóstkowska, Marta and Bukowska, Iwona and Karwicka, Ewa and Raczkowska, Adrianna", title = "OmpR negatively regulates expression of invasin in Yersinia enterocolitica", journal= "Microbiology", year = "2007", volume = "153", number = "8", pages = "2416-2425", doi = "https://doi.org/10.1099/mic.0.2006/003202-0", url = "https://www.microbiologyresearch.org/content/journal/micro/10.1099/mic.0.2006/003202-0", publisher = "Microbiology Society", issn = "1465-2080", type = "Journal Article", keywords = "Cm, chloramphenicol", keywords = "Nal, nalidixic acid", keywords = "Km, kanamycin", keywords = "Tc, tetracycline", abstract = "Invasin, the major adhesion and invasion factor of Yersinia enterocolitica, is encoded by the inv gene, which is regulated by growth phase and in response to a variety of environmental conditions such as temperature, pH and osmolarity. So far, three proteins, RovA, H-NS and YmoA, have been identified as factors regulating the expression of the inv gene in enteropathogenic Yersinia. Here, data from inv′ : : lacZYA chromosomal gene fusion studies are presented indicating that OmpR, the response regulator of the EnvZ/OmpR two-component system, acts to negatively regulate inv expression at the transcriptional level at 25 °C, and that high osmolarity enhances the inhibitory effect of this protein. In a strain lacking OmpR the expression of inv at 25 °C was increased sixfold, but at 37 °C, a temperature known to repress inv expression, this effect was not observed, suggesting that temperature regulation of inv is OmpR-independent. Furthermore, the expression of inv in the ompR background was no longer responsive to increased osmolarity. Complementation with the active ompR allele restored wild-type inv expression in the ompR mutant. In silico analysis of the Y. enterocolitica O : 9 inv promoter sequence revealed the presence of an OmpR consensus binding site located in the −15 to −33 region. OmpR was able to specifically bind to a fragment of the inv promoter containing this putative binding site in electrophoretic mobility shift assays. Thus, OmpR seems to be a repressor of inv in Y. enterocolitica. ", }