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PrfA 导致生物膜形成减少,并导致生物膜形成的单核细胞增生李斯特菌的基因表达模式发生改变。

PrfA led to reduced biofilm formation and contributed to altered gene expression patterns in biofilm-forming Listeria monocytogenes.

机构信息

Hubei Key Laboratory of Genetic Regulation and Integrative Biology, College of Life Science, Central China Normal University, Luo Yu Road 152, Wuhan, 430079, People's Republic of China.

出版信息

Curr Microbiol. 2013 Sep;67(3):372-8. doi: 10.1007/s00284-013-0377-7. Epub 2013 May 8.

DOI:10.1007/s00284-013-0377-7
PMID:23652633
Abstract

The foodborne pathogen Listeria monocytogenes has the ability to develop biofilm in the food-processing environment, which becomes a major concern for food safety. PrfA, a key transcriptional activator that regulates most of the known listerial virulence gene expression, has been shown to promote L. monocytogenes biofilm formation. In this study, the whole-genome microarray was used to identify differentially expressed genes associated with the putative interaction between biofilm formation and PrfA in L. monocytogenes. Comparative transcriptome analyses indicated that over 21.9 % of the L. monocytogenes EGDe genes (627 out of 2,857 predicted) were altered in their expression of biofilm compared to the planktonic phase. These genes were classified into different functional categories which cover most of the biochemical functions encountered in bacterial cells, indicating that L. monocytogenes biofilm formation is probably controlled by a complex regulation network involved in variable genes required for the different biological pathways. Further comparison of gene expression profiles of biofilms between L. monocytogenes EGDe and its PrfA deletion mutant revealed 185 genes associated with PrfA and biofilm formation. Except for 10 genes, transcription levels of 175 genes were completely opposite between ΔprfA and wild-type during the biofilm formation, i.e., up-regulated genes in ΔprfA were down-regulated in the wild-type strain, and vice versa, indicating that loss of PrfA dramatically altered gene expression patterns in L. monocytogenes biofilm and resulted in reduced ability of the biofilm formation.

摘要

食源性病原体单核细胞增生李斯特菌能够在食品加工环境中形成生物膜,这成为食品安全的主要关注点。PrfA 是一种关键的转录激活因子,它调节大多数已知的李斯特菌毒力基因的表达,已被证明能促进单核细胞增生李斯特菌生物膜的形成。在本研究中,使用全基因组微阵列来鉴定与生物膜形成和 PrfA 之间的潜在相互作用相关的差异表达基因。比较转录组分析表明,与浮游期相比,李斯特菌 EGDe 中超过 21.9%的基因(2857 个预测基因中的 627 个)在生物膜形成中的表达发生了改变。这些基因被分为不同的功能类别,涵盖了细菌细胞中遇到的大多数生化功能,表明李斯特菌生物膜的形成可能受到一个复杂的调控网络的控制,该网络涉及到不同生物途径所需的可变基因。进一步比较李斯特菌 EGDe 及其 PrfA 缺失突变体生物膜之间的基因表达谱,发现了 185 个与 PrfA 和生物膜形成相关的基因。除了 10 个基因外,175 个基因在生物膜形成过程中 ΔprfA 和野生型之间的转录水平完全相反,即 ΔprfA 中上调的基因在野生型菌株中下调,反之亦然,这表明 PrfA 的缺失极大地改变了李斯特菌生物膜中的基因表达模式,并导致生物膜形成能力降低。

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