State Key Laboratory of Pathogen and Biosecurity, Beijing Institute of Microbiology and Epidemiology, Beijing 100071, PR China.
BMC Microbiol. 2011 Feb 23;11:39. doi: 10.1186/1471-2180-11-39.
The osmotic regulator OmpR in Escherichia coli regulates differentially the expression of major porin proteins OmpF and OmpC. In Yersinia enterocolitica and Y. pseudotuberculosis, OmpR is required for both virulence and survival within macrophages. However, the phenotypic and regulatory roles of OmpR in Y. pestis are not yet fully understood.
Y. pestis OmpR is involved in building resistance against phagocytosis and controls the adaptation to various stressful conditions met in macrophages. The ompR mutation likely did not affect the virulence of Y. pestis strain 201 that was a human-avirulent enzootic strain. The microarray-based comparative transcriptome analysis disclosed a set of 224 genes whose expressions were affected by the ompR mutation, indicating the global regulatory role of OmpR in Y. pestis. Real-time RT-PCR or lacZ fusion reporter assay further validated 16 OmpR-dependent genes, for which OmpR consensus-like sequences were found within their upstream DNA regions. ompC, F, X, and R were up-regulated dramatically with the increase of medium osmolarity, which was mediated by OmpR occupying the target promoter regions in a tandem manner.
OmpR contributes to the resistance against phagocytosis or survival within macrophages, which is conserved in the pathogenic yersiniae. Y. pestis OmpR regulates ompC, F, X, and R directly through OmpR-promoter DNA association. There is an inducible expressions of the pore-forming proteins OmpF, C, and × at high osmolarity in Y. pestis, in contrast to the reciprocal regulation of them in E. coli. The main difference is that ompF expression is not repressed at high osmolarity in Y. pestis, which is likely due to the absence of a promoter-distal OmpR-binding site for ompF.
大肠杆菌中的渗透调节剂 OmpR 差异调节主要孔蛋白 OmpF 和 OmpC 的表达。在肠侵袭性大肠杆菌和假结核耶尔森菌中，OmpR 既与毒力有关，也与巨噬细胞内的存活有关。然而，OmpR 在鼠疫耶尔森氏菌中的表型和调节作用尚未完全了解。
鼠疫耶尔森氏菌 OmpR 参与了抵御吞噬作用的构建，并控制了适应巨噬细胞中遇到的各种应激条件的能力。ompR 突变不太可能影响鼠疫耶尔森氏菌 201 菌株的毒力，201 菌株是一种人类无致病性的地方病菌株。基于微阵列的比较转录组分析揭示了一组 224 个基因，其表达受到 ompR 突变的影响，表明 OmpR 在鼠疫耶尔森氏菌中具有全局调节作用。实时 RT-PCR 或 lacZ 融合报告基因检测进一步验证了 16 个依赖 OmpR 的基因，在其上游 DNA 区域发现了 OmpR 类似序列的存在。当培养基渗透压增加时，ompC、F、X 和 R 被显著上调，这是通过 OmpR 串联占据靶启动子区域来介导的。
OmpR 有助于抵抗吞噬作用或在巨噬细胞内存活，这在致病性耶尔森氏菌中是保守的。鼠疫耶尔森氏菌 OmpR 通过 OmpR-启动子 DNA 结合直接调节 ompC、F、X 和 R。在高渗透压下，鼠疫耶尔森氏菌中形成孔的蛋白质 OmpF、C 和 × 的表达是诱导的，与大肠杆菌中它们的相互调节相反。主要区别在于在高渗透压下，鼠疫耶尔森氏菌中 ompF 的表达不受抑制，这可能是由于 ompF 缺乏启动子远端 OmpR 结合位点所致。
