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首页> 外文期刊>Environmental microbiology >Role of the LysR-type transcriptional regulator PecT and DNA supercoiling in the thermoregulation of pel genes, the major virulence factors in Dickeya dadantii
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Role of the LysR-type transcriptional regulator PecT and DNA supercoiling in the thermoregulation of pel genes, the major virulence factors in Dickeya dadantii

机译:LysR型转录调节因子PecT和DNA超螺旋在pel基因温度调节中的作用,pel基因是Dickeya dadantii的主要毒力因子

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摘要

Bacteria are colonizers of various environments and host organisms, and they are often subjected to drastic temperature variations. Dickeya dadantii is a pathogen infecting a wide range of plant species. Soft rot, the visible symptom, is mainly due to the production of pectate lyases (Pels) that destroy plant cell walls. The production of Pels is controlled by a complex regulation system that responds to various stimuli, such as the presence of pectin, growth phase and temperature. Despite numerous regulatory studies, the thermoregulation mechanism of Pel production remains unexplained. Here, we show that PecT, a previously identified repressor, modulates pel gene expression in a temperature-dependent manner, and we demonstrate that PecT binding on pel promoters increases concomitantly with temperature. High temperatures relax the DNA in D. dadantii, and remarkably, artificial relaxation of DNA at low temperatures increases PecT binding to DNA. Deletion of pecT augmented the capacity of D. dadantii to initiate soft-rot symptoms at high temperatures. These results reveal that DNA topology and PecT act in concert to fine-tune D. dadantii virulence in response to temperature. This novel combination between DNA topology and a conventional transcriptional regulator extends our understanding of the thermoregulation mechanisms involved in bacterial virulence.
机译:细菌是各种环境和宿主生物的定居者,它们经常经受剧烈的温度变化。 Dickeya dadantii是一种病原体,可感染多种植物。软腐病是可见的症状,主要是由于果胶裂解酶(Pels)的产生破坏了植物细胞壁。 Pels的产生是由复杂的调节系统控制的,该系统对各种刺激(例如果胶的存在,生长期和温度)做出响应。尽管进行了大量的监管研究,但仍无法解释Pel生产的温度调节机制。在这里,我们显示PecT,一种先前鉴定的阻遏物,以依赖温度的方式调节pel基因的表达,并且我们证明pel启动子上的PecT结合随温度增加。高温使达氏梭菌中的DNA松弛,并且值得注意的是,低温下人为地使DNA松弛会增加PecT与DNA的结合。删除pecT可增强D. dadantii在高温下引发软腐病症状的能力。这些结果表明,DNA拓扑结构和PecT协同作用,可根据温度微调D. dadantii毒力。 DNA拓扑结构和常规转录调节剂之间的这种新颖组合扩展了我们对细菌毒力所涉及的温度调节机制的理解。

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