Phenotypic and transcriptional analysis of the osmotic regulator OmpR in Yersinia pestis.

Phenotypic and transcriptional analysis of the osmotic regulator OmpR in Yersinia pestis.
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鼠疫耶尔森氏菌渗透调节因子 OmpR 的表型和转录分析

DOI:
10.1186/1471-2180-11-39
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发表时间:
2011-02-23
期刊:
影响因子:
4.2
通讯作者:
Yang R
Yang R
中科院分区:
生物学3区
文献类型:
--
作者:
Gao H;Zhang Y;Han Y;Yang L;Liu X;Guo Z;Tan Y;Huang X;Zhou D;Yang R

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背景 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。小肠结肠炎耶尔森氏菌和小肠结肠炎耶尔森氏菌均为阳性。假结核,OmpR是巨噬细胞内的毒力和存活所必需的。OmpR在Y.鼠疫还没有被完全了解。 结果 y.鼠疫菌OmpR参与建立对吞噬作用的抗性,并控制对巨噬细胞中遇到的各种应激条件的适应。ompR突变可能不影响Y.鼠疫201株是一种人类无毒的地方流行毒株。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Y中具有全局调节作用。鼠疫实时荧光定量RT-PCR或lacZ融合报告基因检测进一步验证了16个OmpR依赖基因,在其上游DNA区域发现了OmpR一致性序列。ompC、F、X和R随着介质渗透压的增加而显著上调,这是由OmpR以串联方式占据靶启动子区域介导的。 结论 OmpR有助于抵抗巨噬细胞内的吞噬作用或存活,这在致病性耶尔森氏菌中是保守的。y.鼠疫菌OmpR通过OmpR-启动子DNA结合直接调控ompC、F、X和R。在高渗透压条件下,Y细胞中孔形成蛋白OmpF、C和×的表达是可诱导的。pestis之间的相互调节作用,而E.杆菌主要的区别是,ompF的表达在Y的高渗透压下不受抑制。鼠疫杆菌,这可能是由于缺乏启动子远端ompF的OmpR结合位点。
Background 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. Results 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. Conclusion 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.
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