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类核相关蛋白 H-NS 和 FIS 调节植物病原菌迪克氏菌 pel 基因的 DNA 超螺旋响应,pel 基因是该菌的主要毒力因子。

The nucleoid-associated proteins H-NS and FIS modulate the DNA supercoiling response of the pel genes, the major virulence factors in the plant pathogen bacterium Dickeya dadantii.

机构信息

Univ Lyon, F-69622 Lyon, France.

出版信息

Nucleic Acids Res. 2012 May;40(10):4306-19. doi: 10.1093/nar/gks014. Epub 2012 Jan 24.

DOI:10.1093/nar/gks014
PMID:22275524
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3378864/
Abstract

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 can destroy the plant cell walls. Previously we found that the pel gene expression is modulated by H-NS and FIS, two nucleoid-associated proteins (NAPs) modulating the DNA topology. Here, we show that relaxation of the DNA in growing D. dadantii cells decreases the expression of pel genes. Deletion of fis aggravates, whereas that of hns alleviates the negative impact of DNA relaxation on pel expression. We further show that H-NS and FIS directly bind the pelE promoter and that the response of D. dadantii pel genes to stresses that induce DNA relaxation is modulated, although to different extents, by H-NS and FIS. We infer that FIS acts as a repressor buffering the negative impact of DNA relaxation on pel gene transcription, whereas H-NS fine-tunes the response of virulence genes precluding their expression under suboptimal conditions of supercoiling. This novel dependence of H-NS effect on DNA topology expands our understanding of the role of NAPs in regulating the global bacterial gene expression and bacterial pathogenicity.

摘要

软腐病菌 Dickeya dadantii 是一种感染范围广泛的植物病原体。肉眼可见的腐烂症状主要是由于果胶裂解酶(Pels)的产生,这种酶可以破坏植物细胞壁。此前我们发现,pel 基因的表达受 H-NS 和 FIS 这两种与核小体相关的蛋白(NAPs)的调控,它们可以调节 DNA 拓扑结构。在这里,我们表明,生长中的 Dickeya dadantii 细胞中 DNA 的松弛会降低 pel 基因的表达。 fis 缺失会加重这种影响,而 hns 缺失则会减轻 DNA 松弛对 pel 表达的负面影响。我们进一步表明,H-NS 和 FIS 直接结合 pelE 启动子,并且 H-NS 和 FIS 虽然在不同程度上调节了诱导 DNA 松弛的应激对 Dickeya dadantii pel 基因表达的影响。我们推断,FIS 作为一种负调控因子,缓冲了 DNA 松弛对 pel 基因转录的负面影响,而 H-NS 则微调了毒力基因的响应,防止它们在超螺旋不足的条件下表达。这种 H-NS 效应依赖于 DNA 拓扑结构的新发现,扩展了我们对 NAPs 在调节细菌全局基因表达和致病性中的作用的理解。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3162/3378864/902ce6693e99/gks014f7.jpg
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