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四环素调控蛋白家族调节因子brpT调节血链球菌生物膜的形成。

TetR Family Regulator brpT Modulates Biofilm Formation in Streptococcus sanguinis.

作者信息

Liu Jinlin, Stone Victoria N, Ge Xiuchun, Tang Madison, Elrami Fadi, Xu Ping

机构信息

Philips Institute for Oral Health Research, Virginia Commonwealth University, Richmond, Virginia, United States of America.

Department of Microbiology and Immunology, Virginia Commonwealth University, Richmond, Virginia, United States of America.

出版信息

PLoS One. 2017 Jan 3;12(1):e0169301. doi: 10.1371/journal.pone.0169301. eCollection 2017.

Abstract

Biofilms are a key component in bacterial communities providing protection and contributing to infectious diseases. However, mechanisms involved in S. sanguinis biofilm formation have not been clearly elucidated. Here, we report the identification of a novel S. sanguinis TetR repressor, brpT (Biofilm Regulatory Protein TetR), involved in biofilm formation. Deletion of brpT resulted in a significant increase in biofilm formation. Interestingly, the mutant accumulated more water soluble and water insoluble glucans in its biofilm compared to the wild-type and the complemented mutant. The brpT mutation led to an altered biofilm morphology and structure exhibiting a rougher appearance, uneven distribution with more filaments bound to the chains. RNA-sequencing revealed that gtfP, the only glucosyltransferase present in S. sanguinis, was significantly up-regulated. In agreement with these findings, we independently observed that deletion of gtfP in S. sanguinis led to reduced biofilm and low levels of water soluble and insoluble glucans. These results suggest that brpT is involved in the regulation of the gtfP-mediated exopolysaccharide synthesis and controls S. sanguinis biofilm formation. The deletion of brpT may have a potential therapeutic application in regulating S. sanguinis colonization in the oral cavity and the prevention of dental caries.

摘要

生物膜是细菌群落的关键组成部分,可提供保护并导致传染病。然而,血链球菌生物膜形成所涉及的机制尚未得到明确阐明。在此,我们报告了一种参与生物膜形成的新型血链球菌 TetR 阻遏物 brpT(生物膜调节蛋白 TetR)的鉴定。brpT 的缺失导致生物膜形成显著增加。有趣的是,与野生型和互补突变体相比,突变体在其生物膜中积累了更多的水溶性和水不溶性葡聚糖。brpT 突变导致生物膜形态和结构发生改变,外观更粗糙,分布不均匀,有更多细丝附着在链上。RNA 测序显示,血链球菌中唯一的葡糖基转移酶 gtfP 显著上调。与这些发现一致,我们独立观察到血链球菌中 gtfP 的缺失导致生物膜减少以及水溶性和不溶性葡聚糖水平降低。这些结果表明,brpT 参与了 gtfP 介导的胞外多糖合成的调节,并控制血链球菌生物膜的形成。brpT 的缺失在调节血链球菌在口腔中的定植和预防龋齿方面可能具有潜在的治疗应用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/57ca/5207742/33e5fb7d31d6/pone.0169301.g001.jpg

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